肿瘤防治研究2017，Vol.44Issue(7)：447-453,7.DOI:10.3971/j.issn.1000-8578.2017.17.0040
TET1蛋白对人乳腺癌MDA-MB-231细胞株增殖和侵袭能力的影响及其相关机制
Effects of TET1 on Proliferation and Invasion of Human Breast Cancer MDA-MB-231 Cells and Related Mechanism
摘要
Abstract
Objective To investigate the effects of ten-eleven translocation (TET1) on the proliferation,metastasis and invasion of breast cancer MDA-MB-231 cells and possible mechanisns.Methods Breast cancer cell line MDA-MB-231 were stably transfected with recombinant lentiviral expression vector of TET1 and enhanced green fluorescent protein (eGFP).The mRNA and protein expressions of TET1 were detected by Real-time PCR and Western blot.Cell proliferation was detected by CCK-8 assay and flow cytometry was adopted to determine cell cycle distribution.The migration and invasion abilities of cells were detected by wound healing assay and transwell assay.The expression levels of EMT-related protein,such as E-cadherin,N-cadherin,Vimentin and β-catenin,were measured by Western blot and immunofluorescence.Results A stable overexpression of TET1 cell line was successfully obtained (P=0.030).Cell proliferation,migration and invasion abilities were significantly decreased in MDA-MB-23 1-TET1 cells(P＜0.001),compared with control group.The overexpression of TET1 suppressed cell proliferation through inducing G2/M arrest (P=0.002).At the same time,the level of E-cadherin was significantly increased(P＜0.001) and N-cadherin,Vimentin,and β-catenin were decreased(P=0.003,P=0.041,P＜0.001) in MDA-MB-23 1-TET1 cells.TET1 inhibited the nuclear translocation of β-cantenin and then repressed EMT.Conclusion The overexpression of TET1 suppresses the proliferation,migration and invasion abilities of MDA-MB-231 cells by inducing EMT through regulating Wnt/β-catenin pathway in vitro.关键词
TET1/乳腺癌/增殖/侵袭/上皮间充质转化Key words
TET1/Breast cancer/Proliferation/Invasion/Epithelial mesenchymal transition分类
医药卫生引用本文复制引用
张萌萌,李雅琪,张硕,刘运江..TET1蛋白对人乳腺癌MDA-MB-231细胞株增殖和侵袭能力的影响及其相关机制[J].肿瘤防治研究,2017,44(7):447-453,7.基金项目
河北省自然科学基金(H2015206466) （H2015206466）
