Human adipose-derived stem cells(hASCs)are a promising cell type for bone tissue regeneration.Circular RNAs(circRNAs)have been shown to play a critical role in regulating various cell differentiation and involve in me...Human adipose-derived stem cells(hASCs)are a promising cell type for bone tissue regeneration.Circular RNAs(circRNAs)have been shown to play a critical role in regulating various cell differentiation and involve in mesenchymal stem cell osteogenesis.However,how circRNAs regulate hASCs in osteogenesis is still unclear.Herein,we found circ_0003204 was significantly downregulated during osteogenic differentiation of hASCs.Knockdown of circ_0003204 by si RNA or overexpression by lentivirus confirmed circ_0003204 could negatively regulate the osteogenic differentiation of hASCs.We performed dual-luciferase reporting assay and rescue experiments to verify circ_0003204 regulated osteogenic differentiation via sponging miR-370-3p.We predicted and confirmed that miR-370-3p had targets in the 3′-UTR of HDAC4 m RNA.The following rescue experiments indicated that circ_0003204 regulated the osteogenic differentiation of hASCs via miR-370-3p/HDAC4 axis.Subsequent in vivo experiments showed the silencing of circ_0003204 increased the bone formation and promoted the expression of osteogenic-related proteins in a mouse bone defect model,while overexpression of circ_0003204 inhibited bone defect repair.Our findings indicated that circ_0003204 might be a promising target to promote the efficacy of hASCs in repairing bone defects.展开更多
Background:Long-chain non-coding RNA(lncRNA)LINC00609 is a potential tumor suppressor,but the mechanism of action in non-small cell lung cancer(NSCLC)is yet to be understood.Objectives:The effects of LINC00609 on A549...Background:Long-chain non-coding RNA(lncRNA)LINC00609 is a potential tumor suppressor,but the mechanism of action in non-small cell lung cancer(NSCLC)is yet to be understood.Objectives:The effects of LINC00609 on A549 cell proliferation,apoptosis,and cell cycle arrest were investigated.Methods:The LINC00609 levels in NSCLC and normal tissues were analyzed by bioinformatics.Expressions of LINC00609,miR-128-3p,and Rho family GTPase 3(RND3)in NSCLC cells(A549)were determined by qRT-PCR.Bioinformatics analysis predicted target genes and dual-luciferase reporter assays to ensure that LINC00609 targeted miR-128-3p and miR-128-3p targeted RND3.The proliferation of cells was determined using EDU and CCK-8.Flow cytometry was used to evaluate cell apoptosis rate and cell cycle.The western blotting assay identified proteins related to proliferation and apoptosis.Results:In NSCLC tissues,LINC00609 was expressed in low levels,while its high expression was associated with a higher survival rate.LINC00609 affected cell proliferation,apoptosis,cell cycle arrest,and expression of related proteins.Dual-luciferase reporter assay showed that LINC00609 binds specifically to miR-128-3p,and miR-128-3p binds to RND3.MiR-128-3p overexpression could neutralize the effects of LINC00609.A siRNA targeting RND3 could reverse the effect of the miR-128-3p inhibitor.Silencing RND3 resulted in a decrease in apoptosis rate and the number of cells in the S-phase and an increase in the number of cells in the G1-phase.Furthermore,phosphorylation levels of the AKT protein and mTOR protein,and Bcl2 expression,increased;however,the expression of RND3,Bax,and caspase3 decreased.Conclusions:LINC00609 regulated miR-128-3p/RND3 axis to modulate A549 cell proliferation,apoptosis,and cell cycle arrest.In the case of NSCLC,LINC00609 could be a potential target for therapy.展开更多
Using in situ electric-field-modulated anisotropic magnetoresistance measurement, a large reversible and non- volatile in-plane rotation of magnetic easy axis of -35° between the positive and negative electrical ...Using in situ electric-field-modulated anisotropic magnetoresistance measurement, a large reversible and non- volatile in-plane rotation of magnetic easy axis of -35° between the positive and negative electrical poling states is demonstrated in C040Fe40B20//（001）-cut Pb（Mgl/3Nb2/3）O3-25PbTiO3 （PMN-PT）. The specific magneto- electric coupling mechanism therein is experimentally verified to be related to the synchronous in-plane strain rotation induced by 109° ferroelastic domain switching in the （001）-cut PMN-PT substrate.展开更多
Objective:To study the influences of LncRNA H19(H19)on malignant liver tumor cells and elucidate the underlying molecular mechanisms.Methods:H19 expression in liver tumor tissues,matched normal liver tissues,human liv...Objective:To study the influences of LncRNA H19(H19)on malignant liver tumor cells and elucidate the underlying molecular mechanisms.Methods:H19 expression in liver tumor tissues,matched normal liver tissues,human liver malignant tumor cell lines and the human hepatocyte line LO2 was assessed via quantitative RT-PCR.Cell viability analysis and Matrigel invasion analysis were performed to evaluate the effects of H19 on cell proliferation and invasion.Luciferase reporter analysis was carried out to assess the interaction between miR-140-5p and SOS Ras/Rac guanine nucleotide exchange factor 1(SOS1).The influence of H19 on the Ras-MAPK signalling pathway was evaluated by detecting key protein levels via active Ras pull-down analysis and Western blot analysis.Results:H19 expression was lower in liver cancer samples than in matched normal liver tissue samples.H19 overexpression enhanced the proliferation and invasion of HepG2 and SMMC-7721 cells.H19 overexpression increased the level of activated Ras.The expression levels of phosphorylated Raf,phosphorylated ERK and phosphorylated MEK were increased by H19 overexpression.H19 knockdown had the opposite effect.Treatment with a MAPK inhibitor significantly reversed the influence of H19 overexpression on liver malignant tumor cell growth and invasion.The MAPK activator reversed the opposing effects of H19 silencing.H19 overexpression increased the protein level of SOS1,and miR-140-5p directly targeted SOS1.Conclusion:H19 can activate the Ras-MAPK signalling pathway via the miR-140-5p/SOS1 axis in malignant liver tumour cells.展开更多
Weizhou 11-1N Platform is a large wellhead platform with much equipment. After ten years of development, the only low-voltage bus bars on the platform, namely LA, LB and LE bus bars, are already in overload operation,...Weizhou 11-1N Platform is a large wellhead platform with much equipment. After ten years of development, the only low-voltage bus bars on the platform, namely LA, LB and LE bus bars, are already in overload operation, and the chest of drawers of the low-voltage power distribution cabinet has no spare. In view of this problem, considering the follow-up development, according to the next five-year plan, the expansion transformation of low-voltage bus is proposed, i.e. a new low-voltage bus LC bus is added on the original basis, and LA and LC buses are expanded by transforming LA bus and adding ACB switch as bus coupler switch.展开更多
Objective:Transcription factor E2F7 exerts suppressive transcription effects and was validated as highly expressed in hepatocellular carcinoma(HCC)in our previous study.Based on the correlation between E2F7 and the di...Objective:Transcription factor E2F7 exerts suppressive transcription effects and was validated as highly expressed in hepatocellular carcinoma(HCC)in our previous study.Based on the correlation between E2F7 and the dismal clinicopathological features in patients,we investigated the downstream regulators controlled by E2F7 in HCC progression and identified a potential E2F7/miR-218-5p axis facilitating HCC cell growth by stabilizing USP32,one of the important ubiquitin-specific peptidases.Methods:The expression profiles of miR-218-5p and USP32 were detected in HCC cell lines and patients’specimens,combined with the analysis of the public databases.The clinicopathological features of 95 HCC patients were analyzed.Cellular functional experiments through the expression regulation of these genes were conducted in vitro.The chromatin immunoprecipitation and the Dual-luciferase reporter assays were carried out to demonstrate the interaction between the candidate genes.-Results:USP32 was aberrantly overexpressed in HCC,and its high expression was positively associated with poor clinical outcomes and served as an independent risk factor.USP32 depletion impaired HCC cell growth and miR218-5p targeted USP32 mRNA,thereby acting as a suppressive upstream regulator in HCC.E2F7 directly binds to the promoter region of miR-218-5p and suppressively modulates the transcription activity.Modulation of the E2F7/miR-218-5p axis significantly impacts USP32 transcription and HCC cell growth.-Conclusions:USP32 is a pivotal ubiquitin peptidase highly expressed in HCC and facilitates tumor development.The E2F7/miR-218-5p axis functions as an upstream regulatory mechanism that modulates USP32 expression through transcriptional suppression.These genes provide the possibility for innovative targets against HCC.展开更多
基金supported by grants from the National Natural Science Foundation of China(82071150,82170934,81870743,8190104 and 82171001)。
文摘Human adipose-derived stem cells(hASCs)are a promising cell type for bone tissue regeneration.Circular RNAs(circRNAs)have been shown to play a critical role in regulating various cell differentiation and involve in mesenchymal stem cell osteogenesis.However,how circRNAs regulate hASCs in osteogenesis is still unclear.Herein,we found circ_0003204 was significantly downregulated during osteogenic differentiation of hASCs.Knockdown of circ_0003204 by si RNA or overexpression by lentivirus confirmed circ_0003204 could negatively regulate the osteogenic differentiation of hASCs.We performed dual-luciferase reporting assay and rescue experiments to verify circ_0003204 regulated osteogenic differentiation via sponging miR-370-3p.We predicted and confirmed that miR-370-3p had targets in the 3′-UTR of HDAC4 m RNA.The following rescue experiments indicated that circ_0003204 regulated the osteogenic differentiation of hASCs via miR-370-3p/HDAC4 axis.Subsequent in vivo experiments showed the silencing of circ_0003204 increased the bone formation and promoted the expression of osteogenic-related proteins in a mouse bone defect model,while overexpression of circ_0003204 inhibited bone defect repair.Our findings indicated that circ_0003204 might be a promising target to promote the efficacy of hASCs in repairing bone defects.
基金supported by the Fundamental Research Funds for the Central Universities(No.2042021kf1038).
文摘Background:Long-chain non-coding RNA(lncRNA)LINC00609 is a potential tumor suppressor,but the mechanism of action in non-small cell lung cancer(NSCLC)is yet to be understood.Objectives:The effects of LINC00609 on A549 cell proliferation,apoptosis,and cell cycle arrest were investigated.Methods:The LINC00609 levels in NSCLC and normal tissues were analyzed by bioinformatics.Expressions of LINC00609,miR-128-3p,and Rho family GTPase 3(RND3)in NSCLC cells(A549)were determined by qRT-PCR.Bioinformatics analysis predicted target genes and dual-luciferase reporter assays to ensure that LINC00609 targeted miR-128-3p and miR-128-3p targeted RND3.The proliferation of cells was determined using EDU and CCK-8.Flow cytometry was used to evaluate cell apoptosis rate and cell cycle.The western blotting assay identified proteins related to proliferation and apoptosis.Results:In NSCLC tissues,LINC00609 was expressed in low levels,while its high expression was associated with a higher survival rate.LINC00609 affected cell proliferation,apoptosis,cell cycle arrest,and expression of related proteins.Dual-luciferase reporter assay showed that LINC00609 binds specifically to miR-128-3p,and miR-128-3p binds to RND3.MiR-128-3p overexpression could neutralize the effects of LINC00609.A siRNA targeting RND3 could reverse the effect of the miR-128-3p inhibitor.Silencing RND3 resulted in a decrease in apoptosis rate and the number of cells in the S-phase and an increase in the number of cells in the G1-phase.Furthermore,phosphorylation levels of the AKT protein and mTOR protein,and Bcl2 expression,increased;however,the expression of RND3,Bax,and caspase3 decreased.Conclusions:LINC00609 regulated miR-128-3p/RND3 axis to modulate A549 cell proliferation,apoptosis,and cell cycle arrest.In the case of NSCLC,LINC00609 could be a potential target for therapy.
基金Supported by the National Natural Science Foundation of China under Grant Nos 11374010 and 11434009the Fundamental Research Funds for the Central Universities
文摘Using in situ electric-field-modulated anisotropic magnetoresistance measurement, a large reversible and non- volatile in-plane rotation of magnetic easy axis of -35° between the positive and negative electrical poling states is demonstrated in C040Fe40B20//（001）-cut Pb（Mgl/3Nb2/3）O3-25PbTiO3 （PMN-PT）. The specific magneto- electric coupling mechanism therein is experimentally verified to be related to the synchronous in-plane strain rotation induced by 109° ferroelastic domain switching in the （001）-cut PMN-PT substrate.
基金supported by grants from Guangxi Nanning Qingxiu District Key Research and Development Program of Science and Technology Plan(No.2020050)Guangxi Medical and Health Appropriate Technology Development,Promotion and Application Project(No.S2021097)+1 种基金Guangxi Key Research and Development Program(No.AB22080064)Guangxi Natural Science Foundation(No.2017GXNSFAA198126,No.2022GXNSFAA035509).
文摘Objective:To study the influences of LncRNA H19(H19)on malignant liver tumor cells and elucidate the underlying molecular mechanisms.Methods:H19 expression in liver tumor tissues,matched normal liver tissues,human liver malignant tumor cell lines and the human hepatocyte line LO2 was assessed via quantitative RT-PCR.Cell viability analysis and Matrigel invasion analysis were performed to evaluate the effects of H19 on cell proliferation and invasion.Luciferase reporter analysis was carried out to assess the interaction between miR-140-5p and SOS Ras/Rac guanine nucleotide exchange factor 1(SOS1).The influence of H19 on the Ras-MAPK signalling pathway was evaluated by detecting key protein levels via active Ras pull-down analysis and Western blot analysis.Results:H19 expression was lower in liver cancer samples than in matched normal liver tissue samples.H19 overexpression enhanced the proliferation and invasion of HepG2 and SMMC-7721 cells.H19 overexpression increased the level of activated Ras.The expression levels of phosphorylated Raf,phosphorylated ERK and phosphorylated MEK were increased by H19 overexpression.H19 knockdown had the opposite effect.Treatment with a MAPK inhibitor significantly reversed the influence of H19 overexpression on liver malignant tumor cell growth and invasion.The MAPK activator reversed the opposing effects of H19 silencing.H19 overexpression increased the protein level of SOS1,and miR-140-5p directly targeted SOS1.Conclusion:H19 can activate the Ras-MAPK signalling pathway via the miR-140-5p/SOS1 axis in malignant liver tumour cells.
文摘Weizhou 11-1N Platform is a large wellhead platform with much equipment. After ten years of development, the only low-voltage bus bars on the platform, namely LA, LB and LE bus bars, are already in overload operation, and the chest of drawers of the low-voltage power distribution cabinet has no spare. In view of this problem, considering the follow-up development, according to the next five-year plan, the expansion transformation of low-voltage bus is proposed, i.e. a new low-voltage bus LC bus is added on the original basis, and LA and LC buses are expanded by transforming LA bus and adding ACB switch as bus coupler switch.
基金supported by the National Natural Science Foundation of China(Nos.82372603 and 82172900)Shanghai Leading Talent Program of Eastern Talent Plan(No.BJJY2024068)+2 种基金Chinese Society of Clinical Oncology(CSCO)-Chaoyang Oncology Research Foundation(No.Y-Young2021-0015)Research Physician Project from Shanghai Jiao Tong University School of Medicine(No.20191901)Shanghai Pujiang Talent Project,China(No.18PJD029).
文摘Objective:Transcription factor E2F7 exerts suppressive transcription effects and was validated as highly expressed in hepatocellular carcinoma(HCC)in our previous study.Based on the correlation between E2F7 and the dismal clinicopathological features in patients,we investigated the downstream regulators controlled by E2F7 in HCC progression and identified a potential E2F7/miR-218-5p axis facilitating HCC cell growth by stabilizing USP32,one of the important ubiquitin-specific peptidases.Methods:The expression profiles of miR-218-5p and USP32 were detected in HCC cell lines and patients’specimens,combined with the analysis of the public databases.The clinicopathological features of 95 HCC patients were analyzed.Cellular functional experiments through the expression regulation of these genes were conducted in vitro.The chromatin immunoprecipitation and the Dual-luciferase reporter assays were carried out to demonstrate the interaction between the candidate genes.-Results:USP32 was aberrantly overexpressed in HCC,and its high expression was positively associated with poor clinical outcomes and served as an independent risk factor.USP32 depletion impaired HCC cell growth and miR218-5p targeted USP32 mRNA,thereby acting as a suppressive upstream regulator in HCC.E2F7 directly binds to the promoter region of miR-218-5p and suppressively modulates the transcription activity.Modulation of the E2F7/miR-218-5p axis significantly impacts USP32 transcription and HCC cell growth.-Conclusions:USP32 is a pivotal ubiquitin peptidase highly expressed in HCC and facilitates tumor development.The E2F7/miR-218-5p axis functions as an upstream regulatory mechanism that modulates USP32 expression through transcriptional suppression.These genes provide the possibility for innovative targets against HCC.
