Objective To investigate whether there is endogenous neural stem cell proliferation and whether these proliferated neural stem cells represent neural plasticity in the adult rats after cerebral infarction. Methods Cer...Objective To investigate whether there is endogenous neural stem cell proliferation and whether these proliferated neural stem cells represent neural plasticity in the adult rats after cerebral infarction. Methods Cerebral infarction models of rats were established and the dynamic expression of bromodeoxyuridine （BrdU）, BrdU/polysialylated neural cell adhesion molecule （PSA-NCAM） were determined by immunohistochemistry and immunofluorescence staining. BrdU was used to mark dividing neural stem cells. PSA-NCAM was used to mark the plasticity of neural stem cells. Results Compared with controls, the number of BrdU-positive cells in the subventricular zone （SVZ） and hippocampus increased significantly at 1st day after cerebral infarction （P 〈 0. 05 ）, reached maximum at 7th day, decreased markedly at 14th day, but it was still elevated compared with that of the controls （ P 〈 0. 05 ）. The number of BrdU-labeled with PSA-NCAM-positive cells increased significantly at 7th day （ P 〈 0. 05 ）, reached maximum at 14th day, markedly decreased at 28th day, but it was still elevated compared with that of the controls （P 〈 0. 05 ）. It was equal to 60% of the number of BrdU-positive cells in the same period. Conclusion Cerebral infarction may stimulate the proliferation of endogenous neural stem cells in situ and most proliferated neural stem cells represent neural plasticity.展开更多
We report the vegetative proliferation and new phenomenon of ＂secondary proliferated inflorescences＂ In the grass Ischaemum barbatum Retz, as determined by anatomical analysis of prepared sections of inflorescences....We report the vegetative proliferation and new phenomenon of ＂secondary proliferated inflorescences＂ In the grass Ischaemum barbatum Retz, as determined by anatomical analysis of prepared sections of inflorescences. Leaves and shoots could be developed from the original splkelets of Inflorescences and plantlets developed when these shoots were transplanted to moist soil. ＂Secondary proliferated Inflorescences＂ is the first name here because some inflorescences that developed inadequacy are grown from the splkelet on the mother Inflorescence. Our investigation showed that this form of vegetative proliferation and secondary proliferated inflorescences development of L barbatum has arisen following late autumn fires of the previous year. It Is suggested that the sudden onset of a fire could lead to a hormone Imbalance or a chemical induction, which results in ephemeral vegetative proliferation even secondary proliferated inflorescences development in wild populations.展开更多
The published article titled“MicroRNA-133b Inhibits Proliferation,Cellular Migration,and Invasion via Targeting LASP1 in Hepatocarcinoma Cells”has been retracted from Oncology Research,Vol.25,No.8,2017,pp.1269–1282.
Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents.While it is known transforming growth factor-βsignaling is important in embryonic neurogenesis,its role in postn...Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents.While it is known transforming growth factor-βsignaling is important in embryonic neurogenesis,its role in postnatal neurogenesis remains unclear.In this study,to define the precise role of transforming growth factor-βsignaling in postnatal neurogenesis at distinct stages of the neurogenic cascade both in vitro and in vivo,we developed two novel inducible and cell type-specific mouse models to specifically silence transforming growth factor-βsignaling in neural stem cells in(mGFAPcre-ALK5fl/fl-Ai9)or immature neuroblasts in(DCXcreERT2-ALK5fl/fl-Ai9).Our data showed that exogenous transforming growth factor-βtreatment led to inhibition of the proliferation of primary neural stem cells while stimulating their migration.These effects were abolished in activin-like kinase 5(ALK5)knockout primary neural stem cells.Consistent with this,inhibition of transforming growth factor-βsignaling with SB-431542 in wild-type neural stem cells stimulated proliferation while inhibited the migration of neural stem cells.Interestingly,deletion of transforming growth factor-βreceptor in neural stem cells in vivo inhibited the migration of postnatal born neurons in mGFAPcre-ALK5fl/fl-Ai9 mice,while abolishment of transforming growth factor-βsignaling in immature neuroblasts in DCXcreERT2-ALK5fl/fl-Ai9 mice did not affect the migration of these cells in the hippocampus.In summary,our data supports a dual role of transforming growth factor-βsignaling in the proliferation and migration of neural stem cells in vitro.Moreover,our data provides novel insights on cell type-specific-dependent requirements of transforming growth factor-βsignaling on neural stem cell proliferation and migration in vivo.展开更多
The visual system of teleost fish grows continuously,which is a useful model for studying regeneration of the central nervous system.Glial cells are key for this process,but their contribution is still not well define...The visual system of teleost fish grows continuously,which is a useful model for studying regeneration of the central nervous system.Glial cells are key for this process,but their contribution is still not well defined.We followed oligodendrocytes in the visual system of adult zebrafish during regeneration of the optic nerve at 6,24,and 72 hours post-lesion and at 7 and 14 days post-lesion via the sox10:tagRFP transgenic line and confocal microscopy.To understand the changes that these oligodendrocytes undergo during regeneration,we used Sox2 immunohistochemistry,a stem cell marker involved in oligodendrocyte differentiation.We also used the Click-iT™ Plus TUNEL assay to study cell death and a BrdU assay to determine cell proliferation.Before optic nerve crush,sox10:tagRFP oligodendrocytes are located in the retina,in the optic nerve head,and through all the entire optic nerve.Sox2-positive cells are present in the peripheral germinal zone,the mature retina,and the optic nerve.After optic nerve crush,sox10:tagRFP cells disappeared from the optic nerve crush zone,suggesting that they died,although they were not TUNEL positive.Concomitantly,the number of Sox2-positive cells increased around the crushed area,the optic nerve head,and the retina.Then,between 24 hours post-lesion and 14 days post-lesion,double sox10:tagRFP/Sox2-positive cells were detected in the retina,optic nerve head,and whole optic nerve,together with a proliferation response at 72 hours post-lesion.Our results confirm that a degenerating process may occur prior to regeneration.First,sox10:tagRFP oligodendrocytes that surround the degenerated axons stop wrapping them,change their“myelinating oligodendrocyte”morphology to a“nonmyelinating oligodendrocyte”morphology,and die.Then,residual oligodendrocyte progenitor cells in the optic nerve and retina proliferate and differentiate for the purpose of remyelination.As new axons arise from the surviving retinal ganglion cells,new sox10:tagRFP oligodendrocytes arise from residual oligodendrocyte progenitor cells to guide,nourish and myelinate them.Thus,oligodendrocytes play an active role in zebrafish axon regeneration and remyelination.展开更多
Unlike mammals,zebrafish possess a remarkable ability to regenerate their spinal cord after injury,making them an ideal vertebrate model for studying regeneration.While previous research has identified key cell types ...Unlike mammals,zebrafish possess a remarkable ability to regenerate their spinal cord after injury,making them an ideal vertebrate model for studying regeneration.While previous research has identified key cell types involved in this process,the underlying molecular and cellular mechanisms remain largely unexplored.In this study,we used single-cell RNA sequencing to profile distinct cell populations at different stages of spinal cord injury in zebrafish.Our analysis revealed that multiple subpopulations of neurons showed persistent activation of genes associated with axonal regeneration post injury,while molecular signals promoting growth cone collapse were inhibited.Radial glial cells exhibited significant proliferation and differentiation potential post injury,indicating their intrinsic roles in promoting neurogenesis and axonal regeneration,respectively.Additionally,we found that inflammatory factors rapidly decreased in the early stages following spinal cord injury,creating a microenvironment permissive for tissue repair and regeneration.Furthermore,oligodendrocytes lost maturity markers while exhibiting increased proliferation following injury.These findings demonstrated that the rapid and orderly regulation of inflammation,as well as the efficient proliferation and redifferentiation of new neurons and glial cells,enabled zebrafish to reconstruct the spinal cord.This research provides new insights into the cellular transitions and molecular programs that drive spinal cord regeneration,offering promising avenues for future research and therapeutic strategies.展开更多
The early developmental period is a critical window during which brain cells mature and contribute to both brain development and later life functions.Gamma-aminobutyric acid(GABA),recognized as a major neurotransmitte...The early developmental period is a critical window during which brain cells mature and contribute to both brain development and later life functions.Gamma-aminobutyric acid(GABA),recognized as a major neurotransmitter,plays a crucial role in coordinating synapse formation,neuronal proliferation,and migration during this time.展开更多
Objectives:Chromobox 4(CBX4),a polycomb protein family member linked to tumor pathogenesis via dysregulation,has an incompletely defined role in gastric cancer(GC).The study aimed to investigate the role and mechanism...Objectives:Chromobox 4(CBX4),a polycomb protein family member linked to tumor pathogenesis via dysregulation,has an incompletely defined role in gastric cancer(GC).The study aimed to investigate the role and mechanism of CBX4 in GC progression and evaluate its potential as a therapeutic target.Methods:CBX4 expression was assessed in GC tissues vs.adjacent non-cancerous tissues and in GC cell lines vs.normal gastric mucosal epithelial cells.Clinicopathological correlations were analyzed.Functional impacts of CBX4 were determined using knockdown and overexpression models in vitro(cell proliferation,migration,invasion)and in vivo(xenograft tumorigenesis in nude mice).Mechanistic studies evaluatedβ-catenin levels(total and nuclear)and transcriptional activity following CBX4 modulation.The functional dependency on Wnt/β-catenin signaling was tested using the pharmacological inhibitor XAV939 in CBX4-overexpressing cells.Results:CBX4 expression was significantly upregulated in GC tissues and cell lines.Elevated CBX4 levels strongly correlated with aggressive tumor characteristics,including larger tumor size,lymph node metastasis,and advanced Tumor,Node,Metastasis(TNM)stage.Functionally,CBX4 knockdown suppressed GC cell proliferation,migration,invasion in vitro,and tumorigenesis in vivo.Conversely,CBX4 overexpression enhanced these malignant traits.Mechanistically,CBX4 depletion reduced total and nuclearβ-catenin levels and inhibited its transcriptional activity,while CBX4 overexpression had the opposite effect.Critically,XAV939-mediated inhibition of Wnt/β-catenin signaling attenuated the oncogenic effects induced by CBX4 overexpression.Conclusion:CBX4 upregulation promotes GC progression viaβ-catenin signaling activation.The CBX4/β-catenin axis emerges as a promising therapeutic target,offering potential for the development of precision treatment strategies in GC management.展开更多
Background:A significant proportion of patients still cannot benefit from existing targeted therapies and immunotherapies,making the search for new treatment strategies extremely urgent.In this study,we combined integ...Background:A significant proportion of patients still cannot benefit from existing targeted therapies and immunotherapies,making the search for new treatment strategies extremely urgent.In this study,we combined integrate public data analysis with experimental validation to identify novel prognostic biomarkers and therapeutic targets for lung adenocarcinoma(LUAD).Methods:We analyzed RNA and protein databases to assess the expression levels of cytochrome C oxidase 5B(COX5B)in LUAD.Several computational algorithms were employed to investigate the relationship between COX5B and immune infiltration in LUAD.To further elucidate the role of COX5B in LUAD,we utilized multiple experimental approaches,including quantitative reverse transcription PCR assays,western blot,immunohistochemistry,electron microscopy,flow cytometry,and EdU proliferation assays.Results:We revealed that COX5B was significantly elevated in LUAD and positively correlated with poor prognosis of LUAD patients.Analysis of co-expression network indicated that COX5B may take part in the intracellular adenosine triphosphate(ATP)synthesis through the oxidative phosphorylation pathway.There was a negative correlation between COX5B expression and immune infiltration in LUAD.Furthermore,we validated that COX5B levels were significantly elevated in both LUAD tissues and cell lines.Specifically,immunohistochemistry(IHC)assays revealed a 2.32-fold increase of COX5B in tumor tissues compared to that in adjacent normal tissues(p=0.0044).Additionally,COX5B knockdown disrupted the redox homeostasis,ultimately suppressed the proliferation of LUAD cells.Subsequent investigations demonstrated that berberine effectively targeted COX5B,diminishing its protein expression and consequently inhibiting cell proliferation and tumor growth in LUAD.Conclusions:This study established that upregulated COX5B was positive associated with poor patient prognosis in LUAD,elucidating the mechanisms by which berberine targets COX5B to inhibit tumor growth,thereby providing a novel therapeutic target and strategy for the clinical management of LUAD.展开更多
The United States’ investigation into imported Chinese seamless steel pipes intensifies trade frictions while damaging American consumer interests The spike in occurrences and rising intensity of trade protectionism ...The United States’ investigation into imported Chinese seamless steel pipes intensifies trade frictions while damaging American consumer interests The spike in occurrences and rising intensity of trade protectionism has become a growing concern for China’s industry.The U.S. Commerce Department announced its intention展开更多
Peripheral nerve defect repair is a complex process that involves multiple cell types;perineurial cells play a pivotal role.Hair follicle neural crest stem cells promote perineurial cell proliferation and migration vi...Peripheral nerve defect repair is a complex process that involves multiple cell types;perineurial cells play a pivotal role.Hair follicle neural crest stem cells promote perineurial cell proliferation and migration via paracrine signaling;however,their clinical applications are limited by potential risks such as tumorigenesis and xenogeneic immune rejection,which are similar to the risks associated with other stem cell transplantations.The present study therefore focuses on small extracellular vesicles derived from hair follicle neural crest stem cells,which preserve the bioactive properties of the parent cells while avoiding the transplantation-associated risks.In vitro,small extracellular vesicles derived from hair follicle neural crest stem cells significantly enhanced the proliferation,migration,tube formation,and barrier function of perineurial cells,and subsequently upregulated the expression of tight junction proteins.Furthermore,in a rat model of sciatic nerve defects bridged with silicon tubes,treatment with small extracellular vesicles derived from hair follicle neural crest stem cells resulted in higher tight junction protein expression in perineurial cells,thus facilitating neural tissue regeneration.At 10 weeks post-surgery,rats treated with small extracellular vesicles derived from hair follicle neural crest stem cells exhibited improved nerve function recovery and reduced muscle atrophy.Transcriptomic and micro RNA analyses revealed that small extracellular vesicles derived from hair follicle neural crest stem cells deliver mi R-21-5p,which inhibits mothers against decapentaplegic homolog 7 expression,thereby activating the transforming growth factor-β/mothers against decapentaplegic homolog signaling pathway and upregulating hyaluronan synthase 2 expression,and further enhancing tight junction protein expression.Together,our findings indicate that small extracellular vesicles derived from hair follicle neural crest stem cells promote the proliferation,migration,and tight junction protein formation of perineurial cells.These results provide new insights into peripheral nerve regeneration from the perspective of perineurial cells,and present a novel approach for the clinical treatment of peripheral nerve defects.展开更多
Background Thrombin is a multifunctional serine protease that plays a crucial role in hemostasis following tissue injury.In addition to its procoagulation effect, thrombin is also a potent mesenchymal cell mitogen, th...Background Thrombin is a multifunctional serine protease that plays a crucial role in hemostasis following tissue injury.In addition to its procoagulation effect, thrombin is also a potent mesenchymal cell mitogen, therefore it plays important roles in the local proliferation of mesenchymal cells in the tissue repair process. Reactive oxygen species （ROS） can induce some human cells to proliferate at lower rates while at higher concentrations they promote cells to undergo apoptosis or necrosis. Accumulative evidence suggests that thrombin can induce some cells to produce ROS. Based on these observations, we provide a hypothesis that thrombin can stimulate human lung fibroblasts to produce ROS, which play an important role in human lung fibroblast proliferation.Methods ROS were detected in fibroblasts at 30 minutes and 60 minutes following thrombin （20 U/ml） exposure using flow cytometry. The ratio of reduced glutathione/oxidized glutathione （GSH/GSSG） was assayed in lung fibroblasts using a commercial kit following treatment with thrombin at different concentrations. NADPH oxidase and the extracellular regulated kinase1/2 （ERK1/2） signaling pathway were detected by Western blotting after thrombin stimulation to lung fibroblasts.Results Thrombin, at 20 U/ml, stimulated human lung fibroblasts （HLF） to generate ROS in a time dependent manner.The ratio of GSH/GSSG in fibroblasts treated with thrombin showed a significant decrease. NADPH oxidase was activated and the ERK1/2 signal pathway was involved in the proliferation process of fibroblasts treated with thrombin.Conclusion The activation of NADPH oxidase by thrombin leads to the production of ROS, which promotes fibroblasts proliferation via activation of the ERK1/2 signaling pathway.展开更多
Human brain development is a complex process,and animal models often have significant limitations.To address this,researchers have developed pluripotent stem cell-derived three-dimensional structures,known as brain-li...Human brain development is a complex process,and animal models often have significant limitations.To address this,researchers have developed pluripotent stem cell-derived three-dimensional structures,known as brain-like organoids,to more accurately model early human brain development and disease.To enable more consistent and intuitive reproduction of early brain development,in this study,we incorporated forebrain organoid culture technology into the traditional unguided method of brain organoid culture.This involved embedding organoids in matrigel for only 7 days during the rapid expansion phase of the neural epithelium and then removing them from the matrigel for further cultivation,resulting in a new type of human brain organoid system.This cerebral organoid system replicated the temporospatial characteristics of early human brain development,including neuroepithelium derivation,neural progenitor cell production and maintenance,neuron differentiation and migration,and cortical layer patterning and formation,providing more consistent and reproducible organoids for developmental modeling and toxicology testing.As a proof of concept,we applied the heavy metal cadmium to this newly improved organoid system to test whether it could be used to evaluate the neurotoxicity of environmental toxins.Brain organoids exposed to cadmium for 7 or 14 days manifested severe damage and abnormalities in their neurodevelopmental patterns,including bursts of cortical cell death and premature differentiation.Cadmium exposure caused progressive depletion of neural progenitor cells and loss of organoid integrity,accompanied by compensatory cell proliferation at ectopic locations.The convenience,flexibility,and controllability of this newly developed organoid platform make it a powerful and affordable alternative to animal models for use in neurodevelopmental,neurological,and neurotoxicological studies.展开更多
The organotypic retinal explant culture has been established for more than a decade and offers a range of unique advantages compared with in vivo experiments and cell cultures.However,the lack of systematic and contin...The organotypic retinal explant culture has been established for more than a decade and offers a range of unique advantages compared with in vivo experiments and cell cultures.However,the lack of systematic and continuous comparison between in vivo retinal development and the organotypic retinal explant culture makes this model controversial in postnatal retinal development studies.Thus,we aimed to verify the feasibility of using this model for postnatal retinal development studies by comparing it with the in vivo retina.In this study,we showed that postnatal retinal explants undergo normal development,and exhibit a consistent structure and timeline with retinas in vivo.Initially,we used SOX2 and PAX6 immunostaining to identify retinal progenitor cells.We then examined cell proliferation and migration by immunostaining with Ki-67 and doublecortin,respectively.Ki-67-and doublecortin-positive cells decreased in both in vivo and explants during postnatal retinogenesis,and exhibited a high degree of similarity in abundance and distribution between groups.Additionally,we used Ceh-10 homeodomain-containing homolog,glutamate-ammonia ligase(glutamine synthetase),neuronal nuclei,and ionized calcium-binding adapter molecule 1 immunostaining to examine the emergence of bipolar cells,Müller glia,mature neurons,and microglia,respectively.The timing and spatial patterns of the emergence of these cell types were remarkably consistent between in vivo and explant retinas.Our study showed that the organotypic retinal explant culture model had a high degree of consistency with the progression of in vivo early postnatal retina development.The findings confirm the accuracy and credibility of this model and support its use for long-term,systematic,and continuous observation.展开更多
Objective:Verrucous epidermal nevus(VEN),seborrheic keratosis(SK),verruca plana(VP),verruca vulgaris(VV),and nevus sebaceous(NS)are common verrucous proliferative skin diseases with similar clinical appearances,often ...Objective:Verrucous epidermal nevus(VEN),seborrheic keratosis(SK),verruca plana(VP),verruca vulgaris(VV),and nevus sebaceous(NS)are common verrucous proliferative skin diseases with similar clinical appearances,often posing diagnostic challenges.Dermoscopy and reflectance confocal microscopy(RCM)can aid in their differentiation,yet their specific features under these tools have not been systematically described.This study aims to summarize and analyze the dermoscopic and RCM features of VEN,SK,VP,VV,and NS.Methods:A total of 121 patients with histopathologically confirmed verrucous proliferative skin diseases were enrolled.Dermoscopy and RCM imaging was used to observe and analyze the microscopic features of these conditions.Results:Under dermoscopy,the 5 diseases displayed distinct characteristics:VEN typically showed gyriform structures;SK was characterized by gyriform structures,comedo-like openings,and milia-like cysts;VP and VV featured dotted vessels and frogspawn-like structures;NS presented as brownish-yellow globules.RCM revealed shared features such as hyperkeratosis and acanthosis across all 5 diseases.Specific features included gyriform structures and elongated rete ridges in VEN;pseudocysts and gyriform structures in SK;evenly distributed ring-like structures in VP;vacuolated cells and papillomatous proliferation in VV;and frogspawn-like structures in NS.Conclusion:These 5 verrucous proliferative skin conditions exhibit distinguishable features under both dermoscopy and RCM.The combination of these 2 noninvasive imaging modalities holds significant clinical value for the differential diagnosis of verrucous proliferative skin diseases.展开更多
The integration of exercise prescriptions into cancer adjuvant therapy presents challenges stemming from the ambiguity surrounding the precise mechanism through which exercise intervention mitigates the risk of hepato...The integration of exercise prescriptions into cancer adjuvant therapy presents challenges stemming from the ambiguity surrounding the precise mechanism through which exercise intervention mitigates the risk of hepatocellular carcinoma(HCC)mortality and recurrence.Elucidation of this specific mechanism has substantial social and clinical implications.In this study,tumor-bearing mice engaged in voluntary wheel running exhibited a notable decrease in tumor growth,exceeding 30%.Microarray analysis revealed an upregulation of cytokinerelated pathways as a potential explanation for this effect.The inclusion of granulocyte-macrophage colonystimulating factor(GM-CSF)was found to enhance tumor cell proliferation,while the absence of GM-CSF resulted in a marked inhibition of tumor cell growth.The findings suggest that exercise-induced serum from mice can impede the proliferation of mouse tumor cells,with the adipokine chemerin inhibiting the growth factor GM-CSF.Additionally,exercise was found to stimulate chemerin secretion by brown adipose tissue.Chemerin suppression led to a reduction in the inhibition of tumor cell proliferation.The results of this study suggest that exercise may stimulate the release of adipokines from brown adipose tissue,transport them through the blood to the distant tumor microenvironment,and downregulate GM-CSF expression,alleviating tumor immunosuppression in the tumor microenvironment,thereby inhibiting at HCC progression.These findings provide a theoretical basis for incorporating exercise prescription into cancer treatment.展开更多
To explore the potential utilization of Elaeagnus mollis,we conducted a comprehensive assessment of its phytochemical composition,antioxidant properties,cholinesterase inhibition,and anti-HepG2 cell proliferation acti...To explore the potential utilization of Elaeagnus mollis,we conducted a comprehensive assessment of its phytochemical composition,antioxidant properties,cholinesterase inhibition,and anti-HepG2 cell proliferation activity across different plant parts(branch wood,branch bark,and pericarp)using various solvents(water,methanol,ethanol,and n-hexane).Our findings revealed that water extracts displayed superior antioxidant activities in ABTS and RP assays,while methanol extracts exhibited better performance in DPPH and FRAP assays.Moreover,methanol extracts demonstrated the highest effectiveness against anti-HepG2 cell proliferation,whereas n-hexane extracts showed greater efficiency in cholinesterase inhibition.Notably,branch bark extracts exhibited the highest levels of phytochemical compounds,with both branch bark and pericarp extracts demonstrating significant effects in cholinesterase inhibition and anti-HepG2 cell proliferation.Correlation analysis indicated that phytochemical compounds were primarily responsible for the observed biological activities.Overall,extracts from the branch bark and pericarp of E.mollis showed promising potential for antioxidant and anticancer activities,suggesting their suitability for applications in the pharmaceutical industry as health-promoting products.展开更多
In this editorial,we comment on the article by Qin et al,recently published in the World Journal of Gastrointestinal Oncology.Malignant tumors of the digestive tract represent a significant health threat.Kinesin famil...In this editorial,we comment on the article by Qin et al,recently published in the World Journal of Gastrointestinal Oncology.Malignant tumors of the digestive tract represent a significant health threat.Kinesin family member 14(KIF14),a critical kinesin,is pivotal in the proliferation,migration,and invasion of tumor cells.It has emerged as a focal point in recent studies of malignant tumors in the digestive tract.This article reviews the current research on KIF14 within these tumors and details its significant role in tumor cell behaviors,including proliferation,apo-ptosis,migration,invasion,and angiogenesis,alongside the regulatory mechanisms of the associated intracellular signaling pathways.Additionally,it explores the clinical value of KIF14 as a potential biomarker for early diagnosis,disease monitoring,and prognostic evaluation in malignant tumors of the digestive tract.The article concludes by introducing the potential regulatory role of traditional Chinese medicine,aiming to combine the strengths of both modern and traditional medical approaches to enhance treatment outcomes and prognosis for patients with these tumors.展开更多
The presence of endogenous neural stem/progenitor cells in the adult mammalian brain suggests that the central nervous system can be repaired and regenerated after injury.However,whether it is possible to stimulate ne...The presence of endogenous neural stem/progenitor cells in the adult mammalian brain suggests that the central nervous system can be repaired and regenerated after injury.However,whether it is possible to stimulate neurogenesis and reconstruct cortical layers II to VI in non-neurogenic regions,such as the cortex,remains unknown.In this study,we implanted a hyaluronic acid collagen gel loaded with basic fibroblast growth factor into the motor cortex immediately following traumatic injury.Our findings reveal that this gel effectively stimulated the proliferation and migration of endogenous neural stem/progenitor cells,as well as their differentiation into mature and functionally integrated neurons.Importantly,these new neurons reconstructed the architecture of cortical layers II to VI,integrated into the existing neural circuitry,and ultimately led to improved brain function.These findings offer novel insight into potential clinical treatments for traumatic cerebral cortex injuries.展开更多
Background:Transmembrane emp24 trafficking protein 3(TMED3)is associated with the development of several tumors;however,whether TMED3 regulates the progression of prostate cancer remains unclear.Materials and Methods:...Background:Transmembrane emp24 trafficking protein 3(TMED3)is associated with the development of several tumors;however,whether TMED3 regulates the progression of prostate cancer remains unclear.Materials and Methods:Short hairpin RNA was performed to repress TMED3 in prostate cancer cells(DU145 cells)and in a prostate cancer mice model to determine its function in prostate cancer in vitro and in vivo.Results:In the present study,we found that TMED3 was highly expressed in prostate cancer cells.In vitro,shTMED3 treatment suppressed the proliferation,invasion,and migration and promoted the apoptosis of DU145 cells.Additionally,the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed a strong correlation between TMED3 and forkhead box O transcription factor(FOXO)pathway.Furthermore,TMED3 inhibition efficiently decreased FOXO1a and FOXO3a phosphorylation.In vivo,TMED3 downregulation suppressed the apoptosis,growth,and metastasis of prostate cancer cells via FOXO1a and FOXO3a.Conclusion:The present findings show that TMED3 participates in the regulation of prostate cancer progression via FOXO1a and FOXO3a phosphorylation,thereby revealing a novel mechanism underlying prostate cancer development and suggesting that TMED3 inhibition may serve as a novel strategy for prostate cancer treatment.展开更多
基金Supportedby the Early-stage Special FundforImportant Basis Research Projectfrom the Technology Department of China(2002CCAO4400)
文摘Objective To investigate whether there is endogenous neural stem cell proliferation and whether these proliferated neural stem cells represent neural plasticity in the adult rats after cerebral infarction. Methods Cerebral infarction models of rats were established and the dynamic expression of bromodeoxyuridine （BrdU）, BrdU/polysialylated neural cell adhesion molecule （PSA-NCAM） were determined by immunohistochemistry and immunofluorescence staining. BrdU was used to mark dividing neural stem cells. PSA-NCAM was used to mark the plasticity of neural stem cells. Results Compared with controls, the number of BrdU-positive cells in the subventricular zone （SVZ） and hippocampus increased significantly at 1st day after cerebral infarction （P 〈 0. 05 ）, reached maximum at 7th day, decreased markedly at 14th day, but it was still elevated compared with that of the controls （ P 〈 0. 05 ）. The number of BrdU-labeled with PSA-NCAM-positive cells increased significantly at 7th day （ P 〈 0. 05 ）, reached maximum at 14th day, markedly decreased at 28th day, but it was still elevated compared with that of the controls （P 〈 0. 05 ）. It was equal to 60% of the number of BrdU-positive cells in the same period. Conclusion Cerebral infarction may stimulate the proliferation of endogenous neural stem cells in situ and most proliferated neural stem cells represent neural plasticity.
文摘We report the vegetative proliferation and new phenomenon of ＂secondary proliferated inflorescences＂ In the grass Ischaemum barbatum Retz, as determined by anatomical analysis of prepared sections of inflorescences. Leaves and shoots could be developed from the original splkelets of Inflorescences and plantlets developed when these shoots were transplanted to moist soil. ＂Secondary proliferated Inflorescences＂ is the first name here because some inflorescences that developed inadequacy are grown from the splkelet on the mother Inflorescence. Our investigation showed that this form of vegetative proliferation and secondary proliferated inflorescences development of L barbatum has arisen following late autumn fires of the previous year. It Is suggested that the sudden onset of a fire could lead to a hormone Imbalance or a chemical induction, which results in ephemeral vegetative proliferation even secondary proliferated inflorescences development in wild populations.
文摘The published article titled“MicroRNA-133b Inhibits Proliferation,Cellular Migration,and Invasion via Targeting LASP1 in Hepatocarcinoma Cells”has been retracted from Oncology Research,Vol.25,No.8,2017,pp.1269–1282.
基金supported by NIH grants,Nos.R01NS125074,R01AG083164,R01NS107365,and R21NS127177(to YL),1F31NS129204-01A1(to KW)and Albert Ryan Fellowship(to KW).
文摘Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents.While it is known transforming growth factor-βsignaling is important in embryonic neurogenesis,its role in postnatal neurogenesis remains unclear.In this study,to define the precise role of transforming growth factor-βsignaling in postnatal neurogenesis at distinct stages of the neurogenic cascade both in vitro and in vivo,we developed two novel inducible and cell type-specific mouse models to specifically silence transforming growth factor-βsignaling in neural stem cells in(mGFAPcre-ALK5fl/fl-Ai9)or immature neuroblasts in(DCXcreERT2-ALK5fl/fl-Ai9).Our data showed that exogenous transforming growth factor-βtreatment led to inhibition of the proliferation of primary neural stem cells while stimulating their migration.These effects were abolished in activin-like kinase 5(ALK5)knockout primary neural stem cells.Consistent with this,inhibition of transforming growth factor-βsignaling with SB-431542 in wild-type neural stem cells stimulated proliferation while inhibited the migration of neural stem cells.Interestingly,deletion of transforming growth factor-βreceptor in neural stem cells in vivo inhibited the migration of postnatal born neurons in mGFAPcre-ALK5fl/fl-Ai9 mice,while abolishment of transforming growth factor-βsignaling in immature neuroblasts in DCXcreERT2-ALK5fl/fl-Ai9 mice did not affect the migration of these cells in the hippocampus.In summary,our data supports a dual role of transforming growth factor-βsignaling in the proliferation and migration of neural stem cells in vitro.Moreover,our data provides novel insights on cell type-specific-dependent requirements of transforming growth factor-βsignaling on neural stem cell proliferation and migration in vivo.
基金supported by the Lanzadera TCUE and C2 program(Universidad de Salamanca)(to ASL)the Spanish National Research Council(CSIC)funded by the Junta de Castilla y León and co-financed by the European Regional Development Fund(ERDF“Europe drives our growth”):Internationalization Project“CL-EI-2021-08-IBFG Unit of Excellence”,Grant(PID2022-138478OA-100)funded by MICIU/AEI/10.13039/501100011033 and,by FEDER,UE(to MGM)+3 种基金Junta de Castilla y León(SA225P23)Gerencia Regional de Salud(2701/A1/2023)(to AV)the Plan Especial Grado Medicina(USAL)(to CPM)a Ramón y Cajal researcher:Grant RYC2021-033684-I funded by MICIU/AEI/10.13039/501100011033 and,by European Union NextGenerationEU/PRTR.
文摘The visual system of teleost fish grows continuously,which is a useful model for studying regeneration of the central nervous system.Glial cells are key for this process,but their contribution is still not well defined.We followed oligodendrocytes in the visual system of adult zebrafish during regeneration of the optic nerve at 6,24,and 72 hours post-lesion and at 7 and 14 days post-lesion via the sox10:tagRFP transgenic line and confocal microscopy.To understand the changes that these oligodendrocytes undergo during regeneration,we used Sox2 immunohistochemistry,a stem cell marker involved in oligodendrocyte differentiation.We also used the Click-iT™ Plus TUNEL assay to study cell death and a BrdU assay to determine cell proliferation.Before optic nerve crush,sox10:tagRFP oligodendrocytes are located in the retina,in the optic nerve head,and through all the entire optic nerve.Sox2-positive cells are present in the peripheral germinal zone,the mature retina,and the optic nerve.After optic nerve crush,sox10:tagRFP cells disappeared from the optic nerve crush zone,suggesting that they died,although they were not TUNEL positive.Concomitantly,the number of Sox2-positive cells increased around the crushed area,the optic nerve head,and the retina.Then,between 24 hours post-lesion and 14 days post-lesion,double sox10:tagRFP/Sox2-positive cells were detected in the retina,optic nerve head,and whole optic nerve,together with a proliferation response at 72 hours post-lesion.Our results confirm that a degenerating process may occur prior to regeneration.First,sox10:tagRFP oligodendrocytes that surround the degenerated axons stop wrapping them,change their“myelinating oligodendrocyte”morphology to a“nonmyelinating oligodendrocyte”morphology,and die.Then,residual oligodendrocyte progenitor cells in the optic nerve and retina proliferate and differentiate for the purpose of remyelination.As new axons arise from the surviving retinal ganglion cells,new sox10:tagRFP oligodendrocytes arise from residual oligodendrocyte progenitor cells to guide,nourish and myelinate them.Thus,oligodendrocytes play an active role in zebrafish axon regeneration and remyelination.
基金supported by the Jiangsu Province Traditional Chinese Medicine Technology Development Plan Project,Nos.MS2023113(to JC),MS2022090Young and Middle-aged Academic Leaders of Jiangsu Qing-Lan Project(to GL).
文摘Unlike mammals,zebrafish possess a remarkable ability to regenerate their spinal cord after injury,making them an ideal vertebrate model for studying regeneration.While previous research has identified key cell types involved in this process,the underlying molecular and cellular mechanisms remain largely unexplored.In this study,we used single-cell RNA sequencing to profile distinct cell populations at different stages of spinal cord injury in zebrafish.Our analysis revealed that multiple subpopulations of neurons showed persistent activation of genes associated with axonal regeneration post injury,while molecular signals promoting growth cone collapse were inhibited.Radial glial cells exhibited significant proliferation and differentiation potential post injury,indicating their intrinsic roles in promoting neurogenesis and axonal regeneration,respectively.Additionally,we found that inflammatory factors rapidly decreased in the early stages following spinal cord injury,creating a microenvironment permissive for tissue repair and regeneration.Furthermore,oligodendrocytes lost maturity markers while exhibiting increased proliferation following injury.These findings demonstrated that the rapid and orderly regulation of inflammation,as well as the efficient proliferation and redifferentiation of new neurons and glial cells,enabled zebrafish to reconstruct the spinal cord.This research provides new insights into the cellular transitions and molecular programs that drive spinal cord regeneration,offering promising avenues for future research and therapeutic strategies.
基金supported by the Center for Cognition and Sociality,Institute for Basic Science(IBS)(IBS-R001-D2)(to WK).
文摘The early developmental period is a critical window during which brain cells mature and contribute to both brain development and later life functions.Gamma-aminobutyric acid(GABA),recognized as a major neurotransmitter,plays a crucial role in coordinating synapse formation,neuronal proliferation,and migration during this time.
基金funded by the National Natural Science Foundation of China(Grant No.82473566)the Science and Technology Plan Project of Jiangsu Province(Grant No.BE2022728)+2 种基金the Natural Science Foundation of the Higher Education Institutions of Jiangsu Province(Grant No.24KJB320015)the Postgraduate Research&Practice Innovation Program of Jiangsu Province(Grant Nos.SJCX24_1822 and SJCX21_1354)the Soochow University Open Topic from Jiangsu Engineering Laboratory of Novel Functional Polymeric Materials(Grant No.SDGC2312).
文摘Objectives:Chromobox 4(CBX4),a polycomb protein family member linked to tumor pathogenesis via dysregulation,has an incompletely defined role in gastric cancer(GC).The study aimed to investigate the role and mechanism of CBX4 in GC progression and evaluate its potential as a therapeutic target.Methods:CBX4 expression was assessed in GC tissues vs.adjacent non-cancerous tissues and in GC cell lines vs.normal gastric mucosal epithelial cells.Clinicopathological correlations were analyzed.Functional impacts of CBX4 were determined using knockdown and overexpression models in vitro(cell proliferation,migration,invasion)and in vivo(xenograft tumorigenesis in nude mice).Mechanistic studies evaluatedβ-catenin levels(total and nuclear)and transcriptional activity following CBX4 modulation.The functional dependency on Wnt/β-catenin signaling was tested using the pharmacological inhibitor XAV939 in CBX4-overexpressing cells.Results:CBX4 expression was significantly upregulated in GC tissues and cell lines.Elevated CBX4 levels strongly correlated with aggressive tumor characteristics,including larger tumor size,lymph node metastasis,and advanced Tumor,Node,Metastasis(TNM)stage.Functionally,CBX4 knockdown suppressed GC cell proliferation,migration,invasion in vitro,and tumorigenesis in vivo.Conversely,CBX4 overexpression enhanced these malignant traits.Mechanistically,CBX4 depletion reduced total and nuclearβ-catenin levels and inhibited its transcriptional activity,while CBX4 overexpression had the opposite effect.Critically,XAV939-mediated inhibition of Wnt/β-catenin signaling attenuated the oncogenic effects induced by CBX4 overexpression.Conclusion:CBX4 upregulation promotes GC progression viaβ-catenin signaling activation.The CBX4/β-catenin axis emerges as a promising therapeutic target,offering potential for the development of precision treatment strategies in GC management.
基金supported by grants from the Guangxi Natural Science Foundation(2024GXNSFAA010150)the Guangdong Basic and Applied Basic Research Foundation(2022A1515111167).
文摘Background:A significant proportion of patients still cannot benefit from existing targeted therapies and immunotherapies,making the search for new treatment strategies extremely urgent.In this study,we combined integrate public data analysis with experimental validation to identify novel prognostic biomarkers and therapeutic targets for lung adenocarcinoma(LUAD).Methods:We analyzed RNA and protein databases to assess the expression levels of cytochrome C oxidase 5B(COX5B)in LUAD.Several computational algorithms were employed to investigate the relationship between COX5B and immune infiltration in LUAD.To further elucidate the role of COX5B in LUAD,we utilized multiple experimental approaches,including quantitative reverse transcription PCR assays,western blot,immunohistochemistry,electron microscopy,flow cytometry,and EdU proliferation assays.Results:We revealed that COX5B was significantly elevated in LUAD and positively correlated with poor prognosis of LUAD patients.Analysis of co-expression network indicated that COX5B may take part in the intracellular adenosine triphosphate(ATP)synthesis through the oxidative phosphorylation pathway.There was a negative correlation between COX5B expression and immune infiltration in LUAD.Furthermore,we validated that COX5B levels were significantly elevated in both LUAD tissues and cell lines.Specifically,immunohistochemistry(IHC)assays revealed a 2.32-fold increase of COX5B in tumor tissues compared to that in adjacent normal tissues(p=0.0044).Additionally,COX5B knockdown disrupted the redox homeostasis,ultimately suppressed the proliferation of LUAD cells.Subsequent investigations demonstrated that berberine effectively targeted COX5B,diminishing its protein expression and consequently inhibiting cell proliferation and tumor growth in LUAD.Conclusions:This study established that upregulated COX5B was positive associated with poor patient prognosis in LUAD,elucidating the mechanisms by which berberine targets COX5B to inhibit tumor growth,thereby providing a novel therapeutic target and strategy for the clinical management of LUAD.
文摘The United States’ investigation into imported Chinese seamless steel pipes intensifies trade frictions while damaging American consumer interests The spike in occurrences and rising intensity of trade protectionism has become a growing concern for China’s industry.The U.S. Commerce Department announced its intention
基金supported by the National Natural Science Foundation of China,No.81571211(to FL)the Natural Science Foundation of Shanghai,No.22ZR1476800(to CH)。
文摘Peripheral nerve defect repair is a complex process that involves multiple cell types;perineurial cells play a pivotal role.Hair follicle neural crest stem cells promote perineurial cell proliferation and migration via paracrine signaling;however,their clinical applications are limited by potential risks such as tumorigenesis and xenogeneic immune rejection,which are similar to the risks associated with other stem cell transplantations.The present study therefore focuses on small extracellular vesicles derived from hair follicle neural crest stem cells,which preserve the bioactive properties of the parent cells while avoiding the transplantation-associated risks.In vitro,small extracellular vesicles derived from hair follicle neural crest stem cells significantly enhanced the proliferation,migration,tube formation,and barrier function of perineurial cells,and subsequently upregulated the expression of tight junction proteins.Furthermore,in a rat model of sciatic nerve defects bridged with silicon tubes,treatment with small extracellular vesicles derived from hair follicle neural crest stem cells resulted in higher tight junction protein expression in perineurial cells,thus facilitating neural tissue regeneration.At 10 weeks post-surgery,rats treated with small extracellular vesicles derived from hair follicle neural crest stem cells exhibited improved nerve function recovery and reduced muscle atrophy.Transcriptomic and micro RNA analyses revealed that small extracellular vesicles derived from hair follicle neural crest stem cells deliver mi R-21-5p,which inhibits mothers against decapentaplegic homolog 7 expression,thereby activating the transforming growth factor-β/mothers against decapentaplegic homolog signaling pathway and upregulating hyaluronan synthase 2 expression,and further enhancing tight junction protein expression.Together,our findings indicate that small extracellular vesicles derived from hair follicle neural crest stem cells promote the proliferation,migration,and tight junction protein formation of perineurial cells.These results provide new insights into peripheral nerve regeneration from the perspective of perineurial cells,and present a novel approach for the clinical treatment of peripheral nerve defects.
文摘Background Thrombin is a multifunctional serine protease that plays a crucial role in hemostasis following tissue injury.In addition to its procoagulation effect, thrombin is also a potent mesenchymal cell mitogen, therefore it plays important roles in the local proliferation of mesenchymal cells in the tissue repair process. Reactive oxygen species （ROS） can induce some human cells to proliferate at lower rates while at higher concentrations they promote cells to undergo apoptosis or necrosis. Accumulative evidence suggests that thrombin can induce some cells to produce ROS. Based on these observations, we provide a hypothesis that thrombin can stimulate human lung fibroblasts to produce ROS, which play an important role in human lung fibroblast proliferation.Methods ROS were detected in fibroblasts at 30 minutes and 60 minutes following thrombin （20 U/ml） exposure using flow cytometry. The ratio of reduced glutathione/oxidized glutathione （GSH/GSSG） was assayed in lung fibroblasts using a commercial kit following treatment with thrombin at different concentrations. NADPH oxidase and the extracellular regulated kinase1/2 （ERK1/2） signaling pathway were detected by Western blotting after thrombin stimulation to lung fibroblasts.Results Thrombin, at 20 U/ml, stimulated human lung fibroblasts （HLF） to generate ROS in a time dependent manner.The ratio of GSH/GSSG in fibroblasts treated with thrombin showed a significant decrease. NADPH oxidase was activated and the ERK1/2 signal pathway was involved in the proliferation process of fibroblasts treated with thrombin.Conclusion The activation of NADPH oxidase by thrombin leads to the production of ROS, which promotes fibroblasts proliferation via activation of the ERK1/2 signaling pathway.
基金supported by the National Key R&D Program of China,No.2019YFA0110300(to ZG)the National Natural Science Foundation of China,Nos.81773302(to YF),32070862(to ZG).
文摘Human brain development is a complex process,and animal models often have significant limitations.To address this,researchers have developed pluripotent stem cell-derived three-dimensional structures,known as brain-like organoids,to more accurately model early human brain development and disease.To enable more consistent and intuitive reproduction of early brain development,in this study,we incorporated forebrain organoid culture technology into the traditional unguided method of brain organoid culture.This involved embedding organoids in matrigel for only 7 days during the rapid expansion phase of the neural epithelium and then removing them from the matrigel for further cultivation,resulting in a new type of human brain organoid system.This cerebral organoid system replicated the temporospatial characteristics of early human brain development,including neuroepithelium derivation,neural progenitor cell production and maintenance,neuron differentiation and migration,and cortical layer patterning and formation,providing more consistent and reproducible organoids for developmental modeling and toxicology testing.As a proof of concept,we applied the heavy metal cadmium to this newly improved organoid system to test whether it could be used to evaluate the neurotoxicity of environmental toxins.Brain organoids exposed to cadmium for 7 or 14 days manifested severe damage and abnormalities in their neurodevelopmental patterns,including bursts of cortical cell death and premature differentiation.Cadmium exposure caused progressive depletion of neural progenitor cells and loss of organoid integrity,accompanied by compensatory cell proliferation at ectopic locations.The convenience,flexibility,and controllability of this newly developed organoid platform make it a powerful and affordable alternative to animal models for use in neurodevelopmental,neurological,and neurotoxicological studies.
基金supported by the National Natural Science Foundation of China,Nos.81901156(to ZZ),82271200(to ZZ),82171308(to XC)the Fundamental Research Funds for the Central Universities,No.xzy012022035(to ZZ)+1 种基金the Natural Science Foundation of Shaanxi Province,Nos.2021JM-261(to QK),2023-YBSF-303(to ZZ)Traditional Chinese Medicine Project of Shaanxi Province,No.2019-ZZ-JC047(to QK)。
文摘The organotypic retinal explant culture has been established for more than a decade and offers a range of unique advantages compared with in vivo experiments and cell cultures.However,the lack of systematic and continuous comparison between in vivo retinal development and the organotypic retinal explant culture makes this model controversial in postnatal retinal development studies.Thus,we aimed to verify the feasibility of using this model for postnatal retinal development studies by comparing it with the in vivo retina.In this study,we showed that postnatal retinal explants undergo normal development,and exhibit a consistent structure and timeline with retinas in vivo.Initially,we used SOX2 and PAX6 immunostaining to identify retinal progenitor cells.We then examined cell proliferation and migration by immunostaining with Ki-67 and doublecortin,respectively.Ki-67-and doublecortin-positive cells decreased in both in vivo and explants during postnatal retinogenesis,and exhibited a high degree of similarity in abundance and distribution between groups.Additionally,we used Ceh-10 homeodomain-containing homolog,glutamate-ammonia ligase(glutamine synthetase),neuronal nuclei,and ionized calcium-binding adapter molecule 1 immunostaining to examine the emergence of bipolar cells,Müller glia,mature neurons,and microglia,respectively.The timing and spatial patterns of the emergence of these cell types were remarkably consistent between in vivo and explant retinas.Our study showed that the organotypic retinal explant culture model had a high degree of consistency with the progression of in vivo early postnatal retina development.The findings confirm the accuracy and credibility of this model and support its use for long-term,systematic,and continuous observation.
基金supported by the Project of Health Committee of Hunan Province(D202304128868),China.
文摘Objective:Verrucous epidermal nevus(VEN),seborrheic keratosis(SK),verruca plana(VP),verruca vulgaris(VV),and nevus sebaceous(NS)are common verrucous proliferative skin diseases with similar clinical appearances,often posing diagnostic challenges.Dermoscopy and reflectance confocal microscopy(RCM)can aid in their differentiation,yet their specific features under these tools have not been systematically described.This study aims to summarize and analyze the dermoscopic and RCM features of VEN,SK,VP,VV,and NS.Methods:A total of 121 patients with histopathologically confirmed verrucous proliferative skin diseases were enrolled.Dermoscopy and RCM imaging was used to observe and analyze the microscopic features of these conditions.Results:Under dermoscopy,the 5 diseases displayed distinct characteristics:VEN typically showed gyriform structures;SK was characterized by gyriform structures,comedo-like openings,and milia-like cysts;VP and VV featured dotted vessels and frogspawn-like structures;NS presented as brownish-yellow globules.RCM revealed shared features such as hyperkeratosis and acanthosis across all 5 diseases.Specific features included gyriform structures and elongated rete ridges in VEN;pseudocysts and gyriform structures in SK;evenly distributed ring-like structures in VP;vacuolated cells and papillomatous proliferation in VV;and frogspawn-like structures in NS.Conclusion:These 5 verrucous proliferative skin conditions exhibit distinguishable features under both dermoscopy and RCM.The combination of these 2 noninvasive imaging modalities holds significant clinical value for the differential diagnosis of verrucous proliferative skin diseases.
基金supported by Natural Science Foundation of Sichuan Province:2024NSFSC0644.
文摘The integration of exercise prescriptions into cancer adjuvant therapy presents challenges stemming from the ambiguity surrounding the precise mechanism through which exercise intervention mitigates the risk of hepatocellular carcinoma(HCC)mortality and recurrence.Elucidation of this specific mechanism has substantial social and clinical implications.In this study,tumor-bearing mice engaged in voluntary wheel running exhibited a notable decrease in tumor growth,exceeding 30%.Microarray analysis revealed an upregulation of cytokinerelated pathways as a potential explanation for this effect.The inclusion of granulocyte-macrophage colonystimulating factor(GM-CSF)was found to enhance tumor cell proliferation,while the absence of GM-CSF resulted in a marked inhibition of tumor cell growth.The findings suggest that exercise-induced serum from mice can impede the proliferation of mouse tumor cells,with the adipokine chemerin inhibiting the growth factor GM-CSF.Additionally,exercise was found to stimulate chemerin secretion by brown adipose tissue.Chemerin suppression led to a reduction in the inhibition of tumor cell proliferation.The results of this study suggest that exercise may stimulate the release of adipokines from brown adipose tissue,transport them through the blood to the distant tumor microenvironment,and downregulate GM-CSF expression,alleviating tumor immunosuppression in the tumor microenvironment,thereby inhibiting at HCC progression.These findings provide a theoretical basis for incorporating exercise prescription into cancer treatment.
基金National Natural Science Foundation of China(Grant No.31600549).
文摘To explore the potential utilization of Elaeagnus mollis,we conducted a comprehensive assessment of its phytochemical composition,antioxidant properties,cholinesterase inhibition,and anti-HepG2 cell proliferation activity across different plant parts(branch wood,branch bark,and pericarp)using various solvents(water,methanol,ethanol,and n-hexane).Our findings revealed that water extracts displayed superior antioxidant activities in ABTS and RP assays,while methanol extracts exhibited better performance in DPPH and FRAP assays.Moreover,methanol extracts demonstrated the highest effectiveness against anti-HepG2 cell proliferation,whereas n-hexane extracts showed greater efficiency in cholinesterase inhibition.Notably,branch bark extracts exhibited the highest levels of phytochemical compounds,with both branch bark and pericarp extracts demonstrating significant effects in cholinesterase inhibition and anti-HepG2 cell proliferation.Correlation analysis indicated that phytochemical compounds were primarily responsible for the observed biological activities.Overall,extracts from the branch bark and pericarp of E.mollis showed promising potential for antioxidant and anticancer activities,suggesting their suitability for applications in the pharmaceutical industry as health-promoting products.
基金Supported by the 2023 Government-funded Project of the Outstanding Talents Training Program in Clinical Medicine,No.ZF2023165Key Research and Development Projects of Hebei Province,No.18277731D+1 种基金Natural Science Foundation of Hebei Province,No.H202423105Hebei Provincial Administration of Traditional Chinese Medicine,Scientific Research Project,No.2020014.
文摘In this editorial,we comment on the article by Qin et al,recently published in the World Journal of Gastrointestinal Oncology.Malignant tumors of the digestive tract represent a significant health threat.Kinesin family member 14(KIF14),a critical kinesin,is pivotal in the proliferation,migration,and invasion of tumor cells.It has emerged as a focal point in recent studies of malignant tumors in the digestive tract.This article reviews the current research on KIF14 within these tumors and details its significant role in tumor cell behaviors,including proliferation,apo-ptosis,migration,invasion,and angiogenesis,alongside the regulatory mechanisms of the associated intracellular signaling pathways.Additionally,it explores the clinical value of KIF14 as a potential biomarker for early diagnosis,disease monitoring,and prognostic evaluation in malignant tumors of the digestive tract.The article concludes by introducing the potential regulatory role of traditional Chinese medicine,aiming to combine the strengths of both modern and traditional medical approaches to enhance treatment outcomes and prognosis for patients with these tumors.
基金supported by the National Natural Science Foundation of China,Nos.82272171(to ZY),82271403(to XL),81941011(to XL),31971279(to ZY),31730030(to XL)the Natural Science Foundation of Beijing,No.7222004(to HD).
文摘The presence of endogenous neural stem/progenitor cells in the adult mammalian brain suggests that the central nervous system can be repaired and regenerated after injury.However,whether it is possible to stimulate neurogenesis and reconstruct cortical layers II to VI in non-neurogenic regions,such as the cortex,remains unknown.In this study,we implanted a hyaluronic acid collagen gel loaded with basic fibroblast growth factor into the motor cortex immediately following traumatic injury.Our findings reveal that this gel effectively stimulated the proliferation and migration of endogenous neural stem/progenitor cells,as well as their differentiation into mature and functionally integrated neurons.Importantly,these new neurons reconstructed the architecture of cortical layers II to VI,integrated into the existing neural circuitry,and ultimately led to improved brain function.These findings offer novel insight into potential clinical treatments for traumatic cerebral cortex injuries.
基金supported by Guangxi Medical and Health Appropriate Technology Development and Promotion Application Project(S2022022).
文摘Background:Transmembrane emp24 trafficking protein 3(TMED3)is associated with the development of several tumors;however,whether TMED3 regulates the progression of prostate cancer remains unclear.Materials and Methods:Short hairpin RNA was performed to repress TMED3 in prostate cancer cells(DU145 cells)and in a prostate cancer mice model to determine its function in prostate cancer in vitro and in vivo.Results:In the present study,we found that TMED3 was highly expressed in prostate cancer cells.In vitro,shTMED3 treatment suppressed the proliferation,invasion,and migration and promoted the apoptosis of DU145 cells.Additionally,the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed a strong correlation between TMED3 and forkhead box O transcription factor(FOXO)pathway.Furthermore,TMED3 inhibition efficiently decreased FOXO1a and FOXO3a phosphorylation.In vivo,TMED3 downregulation suppressed the apoptosis,growth,and metastasis of prostate cancer cells via FOXO1a and FOXO3a.Conclusion:The present findings show that TMED3 participates in the regulation of prostate cancer progression via FOXO1a and FOXO3a phosphorylation,thereby revealing a novel mechanism underlying prostate cancer development and suggesting that TMED3 inhibition may serve as a novel strategy for prostate cancer treatment.
