miR-137通过靶向EGFR调控宫颈癌细胞增殖和凋亡的作用机制研究

Study on the Mechanism of Action that miR-137 Regulates the Proliferation and Apoptosis of Cervical Cancer Cells by Targeting EGFR

为研究miR-137在宫颈癌细胞中的表达情况,检测其对细胞增殖和凋亡功能的影响并深入探讨其作用机制,采用实时荧光定量PCR检测正常宫颈永生化鳞状细胞及不同宫颈癌细胞中miR-137表达情况;向宫颈癌Ca-Ski细胞中转染miR-137模拟物(miR-137mimics)使其过表达,用CCK8试剂盒检测细胞增殖,用流式技术检测细胞凋亡;并通过软件预测、荧光素酶报告基因及免疫印迹实验验证miR-137靶基因的表达情况。结果发现,miR-137在宫颈癌细胞中表达降低,过表达miR-137能抑制Ca-Ski细胞增殖活力(P<0.01)并提高细胞凋亡水平。深入研究其机制发现表皮生成因子受体(EGFR)为其直接作用靶点,过表达EGFR后可逆转miR-137对宫颈癌细胞生物学功能的影响(P<0.01)。因此,miR-137可以通过靶向调控EGFR,从而抑制宫颈癌细胞增殖并促进细胞凋亡。

In order to study the expression of miR-137 in Cervical Cancer Cells,and examine the effects it has on Proliferation and Apoptosis function and deeply discuss its mechanism of action,adopting real-time fluorescene quantification to examine the expression of miR-137 in normal cervical immortalized squamous cells and different cervical cancer cells;Transfect miR-137 mimics to cervical cancer Ca-Ski cells to make it overexpression,use CCK8 kit to detect Cell proliferation and use streaming technology to detect cell apoptosis.And verify the expression of miR-137 target gene through software prediction,luciferase reporter gene and immunoblotting tests,the results shows that expression of miR-137 in Cervical Cancer Cells was reduced,over-expression of miR-137 can control Ca-Ski cell proliferation activity（P〈0.01）and enhance the level of cell apoptosis.After deeply studying this mechanism,we found epidermal growth factor receptor（EGFR）was target spot of direct action,after overexpression of EGFR,the effects miR-137 has on biological function of Cervical Cancer Cells can be reversed（P〈0.01）.Therefore,miR-137 can control proliferation of Cervical Cancer Cells and promote apoptosis through target regulating EGFR.