miR-26a通过Notch信号通路对NSCLC细胞增殖、凋亡的影响

目的探讨miR-26a通过Notch信号通路对NSCLC细胞增殖、凋亡的影响。方法将NSCLC细胞分为Fz组(未处理)、Fm组(转染miR-26a模拟物)、Fi组(转染miR-26a抑制物)。RT-PCR检测Notch、miR-26a水平,Western blotting检测Notch蛋白表达,Transwell实验检测细胞侵袭,TUNEL检测细胞调亡,免疫组化检测Notch阳性表达。结果RT-PCR结果显示,三组细胞中,Notch mRNA水平为Fi组>Fz组>Fm组,miR-26a水平为Fi组Fz组>Fm组(P<0.05)。Transwell侵袭实验发现显微镜下三组细胞计数为Fi组>Fz组>Fm组,细胞侵袭能力Fi组>Fz组>Fm组(P<0.05)。TUNEL检测发现细胞凋亡水平为Fi组Fz组>Fm组。结论miR-26a抑制剂可通过调控Notch蛋白表达诱导NSCLC细胞凋亡。

Effects of miR-26a on Proliferation and Apoptosis of NSCLC Cells via Notch Signaling Pathway

Objective To investigate the effects of miR-26a on the proliferation and apoptosis of non-small cell lung cancer(NSCLC)cells by regulating Notch signaling pathway.Methods NSCLC cells were divided into three groups:Fz group(NSCLC cells did not undergo any treatment),Fm group(miR-26a mimic)and Fi group(miR-26a inhibitor).The expression of Notch and miR-26a was detected by RTPCR.The Notch protein was detected by Western blotting method.The invasive ability of NSCLC cells was detected by Transwell and the apoptosis was detected by TUNEL.The Notch positive expression was detected by immunohistochemistry.Results Among the three groups,the mRNA level of Notch was the highest in Fi group,but the lowest in Fm group(P<0.05),whereas the mRNA level of miR-26a was the lowest in Fi group,but the highest in Fm group(P<0.05).Western blotting analysis showed that the protein expressions of Notch and Hes1 were the highest in Fi group,but the lowest in Fm group among the three groups(P<0.05).Transwell invasion experiment showed that the invasive ability of cancer cells was stronger in Fi group than in Fz group,but it was weaker in Fm group than in Fz group(P<0.05).TUNEL assay showed that the apoptotic degree of NSCLC cells was the highest in Fm group,but the lowest in Fi group among the three groups(P<0.05).Notch protein was stained brown in the cytoplasm of tumor tissues.The cytoplasm staining of the Fi group was deeper than that of the Fz group,while that of the Fm group was lighter than that of the Fz group(P<0.05).Conclusion miR-26a inhibitor could induce the apoptosis of NSCLC by regulating the Notch protein expression.