目的:探讨转录因子3(TCF3)在子宫内膜癌(EC)中的表达模式及其对癌细胞增殖和侵袭能力的影响。方法:利用The Cancer Genome Atlas(TCGA)数据库分析TCF3在EC中的表达情况及其与患者预后的相关性。通过RNA干扰技术敲减TCF3,结合CCK8增殖实...目的:探讨转录因子3(TCF3)在子宫内膜癌(EC)中的表达模式及其对癌细胞增殖和侵袭能力的影响。方法:利用The Cancer Genome Atlas(TCGA)数据库分析TCF3在EC中的表达情况及其与患者预后的相关性。通过RNA干扰技术敲减TCF3,结合CCK8增殖实验、Transwell侵袭实验和流式细胞仪凋亡、周期检测,评估TCF3对EC细胞生物学行为的影响。结果:EC组织中TCF3表达水平显著高于癌旁组织(Kruskal-Wallis chi-squared=30.53,P<0.05)。TCF3高表达与患者不良预后密切相关(logrank检验,Chi-square statistic=11.63,P<0.05)。t检验显示敲减TCF3显著抑制了细胞增殖(P<0.001)和侵袭能力(P<0.001),并促进了细胞凋亡(P<0.05)。细胞周期分析显示,敲减TCF3并未引起细胞周期的显著变化。结论:TCF3在EC中发挥促进细胞增殖和侵袭的作用,且这一作用与细胞周期调控无关,提示TCF3可能成为治疗EC的潜在靶点。展开更多
Epithelial-mesenchymal transition(EMT)is a vital pathological feature of silica-induced pulmonary fibrosis.However,whether circRNA is involved in the process remains unclear.The present study aimed to investigate the ...Epithelial-mesenchymal transition(EMT)is a vital pathological feature of silica-induced pulmonary fibrosis.However,whether circRNA is involved in the process remains unclear.The present study aimed to investigate the role of circPVT1 in the silica-induced EMT and the underlying mechanisms.We found that an elevated expression of circPVT1 promoted EMT and enhanced the migratory capacity of silica-treated epithelial cells.The isolation of cytoplasmic and nuclear separation assay showed that circPVT1 was predominantly expressed in the cytoplasm.RNA immunoprecipitation assay and RNA pull-down experiment indicated that cytoplasmic-localized circPVT1 was capable of binding to miR-497-5p.Furthermore,we found that miR-497-5p attenuated the silica-induced EMT process by targeting transcription factor 3(TCF3),an E-cadherin transcriptional repressor,in the silica-treated epithelial cells.Collectively,these results reveal a novel role of the circPVT1/miR-497-5p/TCF3 axis in the silica-induced EMT process in lung epithelial cells.Once validated,this finding may provide a potential theoretical basis for the development of interventions and treatments for pulmonary fibrosis.展开更多
基金funded by the National Natural Science Foundation of China(Grant No.82073518).
文摘Epithelial-mesenchymal transition(EMT)is a vital pathological feature of silica-induced pulmonary fibrosis.However,whether circRNA is involved in the process remains unclear.The present study aimed to investigate the role of circPVT1 in the silica-induced EMT and the underlying mechanisms.We found that an elevated expression of circPVT1 promoted EMT and enhanced the migratory capacity of silica-treated epithelial cells.The isolation of cytoplasmic and nuclear separation assay showed that circPVT1 was predominantly expressed in the cytoplasm.RNA immunoprecipitation assay and RNA pull-down experiment indicated that cytoplasmic-localized circPVT1 was capable of binding to miR-497-5p.Furthermore,we found that miR-497-5p attenuated the silica-induced EMT process by targeting transcription factor 3(TCF3),an E-cadherin transcriptional repressor,in the silica-treated epithelial cells.Collectively,these results reveal a novel role of the circPVT1/miR-497-5p/TCF3 axis in the silica-induced EMT process in lung epithelial cells.Once validated,this finding may provide a potential theoretical basis for the development of interventions and treatments for pulmonary fibrosis.
