miR-26a-5p通过靶向THAP2促进子宫内膜癌细胞凋亡

目的:研究miR-26a-5p靶向THAP2对子宫内膜癌细胞凋亡的影响。方法:实时荧光定量RT-PCR法检测子宫内膜癌细胞中miR-26a-5p表达水平。构建以慢病毒为载体的miR-26a-5p过表达和干扰质粒,分别转染子宫内膜癌细胞系Ishikawa与KLE,实时荧光定量RT-PCR法检测miR-26a-5p及下游分子THAP2转录水平。流式细胞技术分析miR-26a-5p表达对子宫内膜癌细胞凋亡的影响。结果:子宫内膜癌细胞Ishikawa与KLE均表达miR-26a-5p;miR-26a-5p过表达能增加THAP2的转录水平,促进子宫内膜癌细胞凋亡;miR-26a-5p下调能抑制THAP2的转录水平,抑制子宫内膜癌细胞凋亡。结论:miR-26a-5p可提高THAP2的转录水平,促进子宫内膜癌细胞凋亡,明确这种调控机制可能为子宫内膜癌预防诊断和治疗带来新的契机。

miR-26a-5p promotes the apoptosis of endometrial cancer cells via targeting THAP2

Objective:To investigate the miR-26a-5p regulates THAP2 further influences apoptosis of endometrial cancer cells.Method:Level of miR-26a-5p in endometrial cancer cells was analyzed by real-time fluorescence quantification.miR-26a-5p overexpress and inhibit plasmids were designed.After transfecting lentivirus into endometrial cancer cells,mRNA level of miR-26a-5p and THAP2 were analyzed by real-time fluorescence quantification.The influence of endometrial cancer cells apoptosis by miR-26a-5p changes was analyzed by flow cytometry.Result:There was the expression of miR-26a-5p in endometrial cancer cell lines:Ishikawa and KLE.Lentivirus transfection changed mRNA level of miR-26a-5p obviously in endometrial cancer cells.Up regulation of miR-26a-5p can enhance mRNA level of THAP2 and accelerate apoptosis of endometrial cancer cells.Down regulation of miR-26a-5p can reduce mRNA level of THAP2 and inhibit apoptosis of endometrial cancer cells.Conclusion:miR-26a-5p can promote mRNA level of THAP2,and then induce apoptosis of endometrial cancer cells,which may play an important role in prevention,diagnose and therapy of endometrial cancers.