Published:18 July 2025 The published article titled“Inhibition of Liver Carcinoma Cell Invasion and Metastasis by Knockdown of Cullin7 In Vitro and In Vivo”has been retracted from Oncology Research,Vol.23,No.4,2015,...Published:18 July 2025 The published article titled“Inhibition of Liver Carcinoma Cell Invasion and Metastasis by Knockdown of Cullin7 In Vitro and In Vivo”has been retracted from Oncology Research,Vol.23,No.4,2015,pp.171–181.DOI:10.3727/096504016X14519995067562 URL:https://www.techscience.com/or/v23n4/57554 Following the publication,concerns have been raised about a number of figures in this article.An unexpected area of similarity was identified in terms of the cellular data,where the results from differently performed experiments were intended to have been shown,although the areas immediately surrounding this area featured comparatively different distributions of cells.In addition,the western blots in this article were presented with atypical,unusually shaped and possibly anomalous protein bands in many cases.展开更多
Objective:To investigate the prevalence,mechanisms,and trends of knockdown resistance(kdr)in Anopheles(An.)culicifacies and its impact on the efficacy of organochlorine and other insecticides.Methods:A systematic revi...Objective:To investigate the prevalence,mechanisms,and trends of knockdown resistance(kdr)in Anopheles(An.)culicifacies and its impact on the efficacy of organochlorine and other insecticides.Methods:A systematic review was conducted based on PRISMA guidelines,extracting data from biooan.org,Embase,ProQuest,PubMed,Scopus,and Web of Science without a time limit until the end of 2022.Articles meeting the inclusion criteria were assessed using the STROBE checklist.Data on kdr mutations,insecticide resistance,and effectiveness were analyzed across eight selected studies from various regions.Results:The review revealed widespread kdr-mediated resistance in An.culicifacies,primarily against dichloro-diphenyl-trichloroethane(DDT),persisting even decades after discontinued use.Key kdr mutations,including L1014F and L1014S,were identified.Resistance to deltamethrin was less stable,with increased sensitivity observed after short-term discontinuation.The findings underscore the vector's sustained resistance to organochlorine insecticides and relative sensitivity to pyrethroids.Conclusions:Stable kdr resistance in An.culicifacies to organochlorine insecticides highlights the need for periodic susceptibility assessments and strategic rotation or combination of insecticides to combat malaria effectively and prevent the development of resistance.展开更多
CRISPR-Cas endonucleases mediate prokaryotic adaptive immunity by targeting foreign nucleic acids.CRISPR/Cas13b is a class 2 type VI-B ribonuclease that targets and cleaves single-stranded RNA.It exhibits higher RNA i...CRISPR-Cas endonucleases mediate prokaryotic adaptive immunity by targeting foreign nucleic acids.CRISPR/Cas13b is a class 2 type VI-B ribonuclease that targets and cleaves single-stranded RNA.It exhibits higher RNA interference activity than Cas13a and Cas13c and causes fewer collateral effects than RxCas13d in mammalian cells.However,a programmable CRISPR/Cas13b-mediated RNA interference system for endogenous transcripts in rice has not yet been established.Here,we developed a CRISPR/Cas13b-mediated system to target endogenous transcripts in rice.Our CRISPR/Cas13b system could inhibit multiple endogenous mRNAs simultaneously.In addition,this system efficiently repressed endogenous long noncoding RNAs with more than 50% inhibition in stable transgenic plants.Furthermore,we found only weak collateral effects of the CRISPR/Cas13b-mediated system at the transcriptome-wide level,and no difference in the agronomic traits of stable transgenic rice in the field.We present a programmable CRISPR/Cas13b-mediated knockdown system for rice,offering a potential biotechnological tool for functional genomics and crop improvement.展开更多
BACKGROUND The role of Sm-like 5(LSM5)in colon cancer has not been determined.In this study,we investigated the role of LSM5 in progression of colon cancer and the potential underlying mechanism involved.AIM To determ...BACKGROUND The role of Sm-like 5(LSM5)in colon cancer has not been determined.In this study,we investigated the role of LSM5 in progression of colon cancer and the potential underlying mechanism involved.AIM To determine the role of LSM5 in the progression of colon cancer and the potential underlying mechanism involved.METHODS The Gene Expression Profiling Interactive Analysis database and the Human Protein Atlas website were used for LSM5 expression analysis and prognosis analysis.Real-time quantitative polymerase chain reaction and Western blotting were utilized to detect the expression of mRNAs and proteins.A lentivirus targeting LSM5 was constructed and transfected into colon cancer cells to silence LSM5 expression.Proliferation and apoptosis assays were also conducted to evaluate the growth of the colon cancer cells.Human GeneChip assay and bioinformatics analysis were performed to identify the potential underlying mechanism of LSM5 in colon cancer.RESULTS LSM5 was highly expressed in tumor tissue and colon cancer cells.A high expression level of LSM5 was related to poor prognosis in patients with colon cancer.Knockdown of LSM5 suppressed proliferation and promoted apoptosis in colon cancer cells.Silencing of LSM5 also facilitates the expression of p53,cyclin-dependent kinase inhibitor 1A(CDKN1A)and tumor necrosis factor receptor superfamily 10B(TNFRSF10B).The inhibitory effect of LSM5 knockdown on the growth of colon cancer cells was associated with the upregulation of p53,CDKN1A and TNFRSF10B.CONCLUSION LSM5 knockdown inhibited the proliferation and facilitated the apoptosis of colon cancer cells by upregulating p53,CDKN1A and TNFRSF10B.展开更多
背景:溶质载体家族1成员5(solute carrier family 1 member 5,SLC1A5)在多种疾病中发挥了潜在作用,但确切作用机制尚不清楚。构建稳定的SLC1A5过表达和敲低细胞模型可为深入研究SLC1A5在疾病中的确切作用机制以及发现潜在治疗靶点提供...背景:溶质载体家族1成员5(solute carrier family 1 member 5,SLC1A5)在多种疾病中发挥了潜在作用,但确切作用机制尚不清楚。构建稳定的SLC1A5过表达和敲低细胞模型可为深入研究SLC1A5在疾病中的确切作用机制以及发现潜在治疗靶点提供有力的实验工具。目的:构建小鼠SLC1A5过表达和敲低的慢病毒载体,以建立稳定转染的RAW264.7细胞株,为深入探讨SLC1A5在炎症中的作用提供实验基础。方法:根据SLC1A5基因序列设计合成引物并使用聚合酶链反应扩增该基因片段。将目的基因定向接入经Age I/Nhe I酶切的载体质粒GV492中构建重组慢病毒质粒,对阳性克隆进一步筛选后测序比对结果;pHelper1.0质粒载体、pHelper2.0质粒载体、目的质粒载体与293T细胞共同培养并转染,获得慢病毒原液进行包装和滴度测定;在此基础上,通过体外培养RAW264.7细胞,确定嘌呤霉素工作质量浓度;不同滴度的慢病毒分别与RAW264.7细胞共同培养,根据荧光强度确定转染效率;用嘌呤霉素挑选出稳定转染细胞,实时荧光定量聚合酶链反应和蛋白免疫印迹方法检测稳定转染细胞株的SLC1A5基因和蛋白表达水平。结果与结论:(1)测序序列与目的序列一致提示重组慢病毒载体构建成功;(2)过表达SLC1A5慢病毒的滴度为1×10~9 TU/mL,敲低SLC1A5慢病毒的滴度为3×10~9 TU/mL;(3)确定RAW264.7细胞嘌呤霉素工作质量浓度为3μg/mL;(4)过表达/敲低SLC1A5慢病毒转染RAW264.7细胞的最佳条件皆为HiTransG P转染增强液且感染复数值等于50;(5)过表达SLC1A5稳转细胞株中SLC1A5基因和蛋白的表达量明显上调,而敲低SLC1A5稳转细胞株中SLC1A5基因和蛋白的表达量显著下调。结果表明,成功构建了小鼠SLC1A5过表达和敲低的慢病毒载体并获得稳定转染的RAW264.7细胞株。展开更多
Human dental pulp cells （hDPCs） possess the capacity to differentiate into odontoblast-like cells and generate reparative dentin in response to exogenous stimuli or injury. Ten-eleven translocation 1 （TET1） is a n...Human dental pulp cells （hDPCs） possess the capacity to differentiate into odontoblast-like cells and generate reparative dentin in response to exogenous stimuli or injury. Ten-eleven translocation 1 （TET1） is a novel DNA methyldioxygenase that plays an important role in the promotion of DNA demethylation and transcriptional regulation in several cell lines. However, the role of TET1 in the biological functions of hDPCs is unknown. To investigate the effect of TET1 on the proliferation and odontogenic differentiation potential of hDPCs, a recombinant shRNA lentiviral vector was used to knock down TET1 expression in hDPCs. Following TET1 knockdown, TET1 was significantly downregulated at both the mRNA and protein levels. Proliferation of the hDPCs was suppressed in the TET1 knockdown groups. Alkaline phosphatase activity, the formation of mineralized nodules, and the expression levels of DSPP and DMP1 were all reduced in the TETl-knockdown hDPCs undergoing odontogenic differentiation. Based on these results, we concluded that TET1 knockdown can prevent the proliferation and odontogenic differentiation of hDPCs, which suggests that TET1 may play an important role in dental pulp repair and regeneration.展开更多
The micro RNA（mi RNA） let-7 was one of the first mi RNAs to be discovered, and is highly conserved and widely expressed among species. let-7 expression increases in brain tissue after cerebral ischemia/reperfusion i...The micro RNA（mi RNA） let-7 was one of the first mi RNAs to be discovered, and is highly conserved and widely expressed among species. let-7 expression increases in brain tissue after cerebral ischemia/reperfusion injury; however, no studies have reported let-7 effects on nerve injury after cerebral ischemia/reperfusion injury. To investigate the effects of let-7 gene knockdown on cerebral ischemia/reperfusion injury, we established a rat model of cerebral ischemia/reperfusion injury. Quantitative reverse transcription-polymerase chain reaction demonstrated that 12 hours after cerebral ischemia/reperfusion injury, let-7 expression was up-regulated, peaked at 24 hours, and was still higher than that in control rats after 72 hours. Let-7 gene knockdown in rats suppressed microglial activation and inflammatory factor release, reduced neuronal apoptosis and infarct volume in brain tissue after cerebral ischemia/reperfusion injury. Western blot assays and luciferase assays revealed that mitogen-activated protein kinase phosphatase-1（MKP1） is a direct target of let-7. Let-7 enhanced phosphorylated p38 mitogen-activated protein kinase（MAPK） and c-Jun N-terminal kinase（JNK） expression by down-regulating MKP1. These findings suggest that knockdown of let-7 inhibited the activation of p38 MAPK and JNK signaling pathways by up-regulating MKP1 expression, reduced apoptosis and the inflammatory reaction, and exerted a neuroprotective effect following cerebral ischemia/reperfusion injury.展开更多
文摘Published:18 July 2025 The published article titled“Inhibition of Liver Carcinoma Cell Invasion and Metastasis by Knockdown of Cullin7 In Vitro and In Vivo”has been retracted from Oncology Research,Vol.23,No.4,2015,pp.171–181.DOI:10.3727/096504016X14519995067562 URL:https://www.techscience.com/or/v23n4/57554 Following the publication,concerns have been raised about a number of figures in this article.An unexpected area of similarity was identified in terms of the cellular data,where the results from differently performed experiments were intended to have been shown,although the areas immediately surrounding this area featured comparatively different distributions of cells.In addition,the western blots in this article were presented with atypical,unusually shaped and possibly anomalous protein bands in many cases.
文摘Objective:To investigate the prevalence,mechanisms,and trends of knockdown resistance(kdr)in Anopheles(An.)culicifacies and its impact on the efficacy of organochlorine and other insecticides.Methods:A systematic review was conducted based on PRISMA guidelines,extracting data from biooan.org,Embase,ProQuest,PubMed,Scopus,and Web of Science without a time limit until the end of 2022.Articles meeting the inclusion criteria were assessed using the STROBE checklist.Data on kdr mutations,insecticide resistance,and effectiveness were analyzed across eight selected studies from various regions.Results:The review revealed widespread kdr-mediated resistance in An.culicifacies,primarily against dichloro-diphenyl-trichloroethane(DDT),persisting even decades after discontinued use.Key kdr mutations,including L1014F and L1014S,were identified.Resistance to deltamethrin was less stable,with increased sensitivity observed after short-term discontinuation.The findings underscore the vector's sustained resistance to organochlorine insecticides and relative sensitivity to pyrethroids.Conclusions:Stable kdr resistance in An.culicifacies to organochlorine insecticides highlights the need for periodic susceptibility assessments and strategic rotation or combination of insecticides to combat malaria effectively and prevent the development of resistance.
基金supported by the Natural Science Foundation of Zhejiang Province,China(Grant Nos.LZ22C150002 and LR24C150001)the National Key Research and Development Program of China(Grant Nos.2021YFF1000402 and 2022YFD1401600)+1 种基金the National Natural Science Foundation of China(Grant No.32170262)the Fundamental Research Funds for the Central Universities,China(Grant No.K20240124).
文摘CRISPR-Cas endonucleases mediate prokaryotic adaptive immunity by targeting foreign nucleic acids.CRISPR/Cas13b is a class 2 type VI-B ribonuclease that targets and cleaves single-stranded RNA.It exhibits higher RNA interference activity than Cas13a and Cas13c and causes fewer collateral effects than RxCas13d in mammalian cells.However,a programmable CRISPR/Cas13b-mediated RNA interference system for endogenous transcripts in rice has not yet been established.Here,we developed a CRISPR/Cas13b-mediated system to target endogenous transcripts in rice.Our CRISPR/Cas13b system could inhibit multiple endogenous mRNAs simultaneously.In addition,this system efficiently repressed endogenous long noncoding RNAs with more than 50% inhibition in stable transgenic plants.Furthermore,we found only weak collateral effects of the CRISPR/Cas13b-mediated system at the transcriptome-wide level,and no difference in the agronomic traits of stable transgenic rice in the field.We present a programmable CRISPR/Cas13b-mediated knockdown system for rice,offering a potential biotechnological tool for functional genomics and crop improvement.
基金Supported by Natural Science Basic Research Program of Shaanxi Province,No.2021JM-256.
文摘BACKGROUND The role of Sm-like 5(LSM5)in colon cancer has not been determined.In this study,we investigated the role of LSM5 in progression of colon cancer and the potential underlying mechanism involved.AIM To determine the role of LSM5 in the progression of colon cancer and the potential underlying mechanism involved.METHODS The Gene Expression Profiling Interactive Analysis database and the Human Protein Atlas website were used for LSM5 expression analysis and prognosis analysis.Real-time quantitative polymerase chain reaction and Western blotting were utilized to detect the expression of mRNAs and proteins.A lentivirus targeting LSM5 was constructed and transfected into colon cancer cells to silence LSM5 expression.Proliferation and apoptosis assays were also conducted to evaluate the growth of the colon cancer cells.Human GeneChip assay and bioinformatics analysis were performed to identify the potential underlying mechanism of LSM5 in colon cancer.RESULTS LSM5 was highly expressed in tumor tissue and colon cancer cells.A high expression level of LSM5 was related to poor prognosis in patients with colon cancer.Knockdown of LSM5 suppressed proliferation and promoted apoptosis in colon cancer cells.Silencing of LSM5 also facilitates the expression of p53,cyclin-dependent kinase inhibitor 1A(CDKN1A)and tumor necrosis factor receptor superfamily 10B(TNFRSF10B).The inhibitory effect of LSM5 knockdown on the growth of colon cancer cells was associated with the upregulation of p53,CDKN1A and TNFRSF10B.CONCLUSION LSM5 knockdown inhibited the proliferation and facilitated the apoptosis of colon cancer cells by upregulating p53,CDKN1A and TNFRSF10B.
基金supported by the National Nature Science Foundation of China (grant no.81570971)
文摘Human dental pulp cells （hDPCs） possess the capacity to differentiate into odontoblast-like cells and generate reparative dentin in response to exogenous stimuli or injury. Ten-eleven translocation 1 （TET1） is a novel DNA methyldioxygenase that plays an important role in the promotion of DNA demethylation and transcriptional regulation in several cell lines. However, the role of TET1 in the biological functions of hDPCs is unknown. To investigate the effect of TET1 on the proliferation and odontogenic differentiation potential of hDPCs, a recombinant shRNA lentiviral vector was used to knock down TET1 expression in hDPCs. Following TET1 knockdown, TET1 was significantly downregulated at both the mRNA and protein levels. Proliferation of the hDPCs was suppressed in the TET1 knockdown groups. Alkaline phosphatase activity, the formation of mineralized nodules, and the expression levels of DSPP and DMP1 were all reduced in the TETl-knockdown hDPCs undergoing odontogenic differentiation. Based on these results, we concluded that TET1 knockdown can prevent the proliferation and odontogenic differentiation of hDPCs, which suggests that TET1 may play an important role in dental pulp repair and regeneration.
基金supported by the National Natural Science Foundation of China,No.81460193
文摘The micro RNA（mi RNA） let-7 was one of the first mi RNAs to be discovered, and is highly conserved and widely expressed among species. let-7 expression increases in brain tissue after cerebral ischemia/reperfusion injury; however, no studies have reported let-7 effects on nerve injury after cerebral ischemia/reperfusion injury. To investigate the effects of let-7 gene knockdown on cerebral ischemia/reperfusion injury, we established a rat model of cerebral ischemia/reperfusion injury. Quantitative reverse transcription-polymerase chain reaction demonstrated that 12 hours after cerebral ischemia/reperfusion injury, let-7 expression was up-regulated, peaked at 24 hours, and was still higher than that in control rats after 72 hours. Let-7 gene knockdown in rats suppressed microglial activation and inflammatory factor release, reduced neuronal apoptosis and infarct volume in brain tissue after cerebral ischemia/reperfusion injury. Western blot assays and luciferase assays revealed that mitogen-activated protein kinase phosphatase-1（MKP1） is a direct target of let-7. Let-7 enhanced phosphorylated p38 mitogen-activated protein kinase（MAPK） and c-Jun N-terminal kinase（JNK） expression by down-regulating MKP1. These findings suggest that knockdown of let-7 inhibited the activation of p38 MAPK and JNK signaling pathways by up-regulating MKP1 expression, reduced apoptosis and the inflammatory reaction, and exerted a neuroprotective effect following cerebral ischemia/reperfusion injury.
