miR-26a下调TET抑制人宫颈癌HeLa细胞增殖与侵袭

miR-26a inhibits the growth and invasion of human cervical cancer HeLa cells by down-regulating TET

摘要:

目的探讨TET对宫颈癌HeLa细胞增殖和侵袭的作用及其调控机制。方法siRNA敲低宫颈癌HeLa细胞中TET的表达。细胞计数法、克隆形成实验、Transwell侵袭实验检测TET对宫颈癌HeLa细胞增殖、克隆形成及侵袭能力的影响。TargetScan软件预测TET与miR-26a之间的结合位点,qRT-PCR和双荧光素酶报告基因实验检测TET与miR-26之间的关系。结果TET敲低抑制宫颈癌HeLa细胞增殖、克隆形成及侵袭能力。经预测miR-26a与TET1、TET2和TET3之间均存在结合位点；共转染野生型TET和miR-26a模拟物可降低荧光素酶活性；转染miR-26a抑制HeLa细胞中TET的表达。结论miR-26a通过下调TET1、TET2和TET3的表达而抑制宫颈癌HeLa细胞增殖与侵袭能力。

Abstract:

To investigate the effects of TET on the growth and invasion of cervical cancer HeLa cells and its regulation mechanism. MethodsThe expression of TET was knocked down by siRNA in cervical cancer cell HeLa. The effect of TET on the growth, clone formation and invasion ability of cervical cancer HeLa cells were detected by cell counting, clonal formation assay and Transwell invasion assay. TargetScan software was used to predict the binding site between TET and miR-26a. qRT-PCR and dual luciferase reporter gene experiments were used to detect the relationship between TET and miR-26. ResultsTET knockdown inhibited the growth, clonal formation and invasion ability of cervical cancer HeLa cells. It was predicted that there were binding sites between miR-26a and TET1, TET2 and TET3.Co-transfection of wild-type TET and miR-26a mimics reduced luciferase activity. Transfection of miR-26a inhibited the expression of TET in HeLa cells. ConclusionmiR-26a can inhibit the growth and invasion ability of cervical cancer HeLa cells by down-regulating the expression of TET1, TET2 and TET3.