MiR-451靶向调控SIRT1通路对胃癌细胞增殖的作用机制研究  被引量:1

Mechanism of MiR-451 Targeting Regulation of SIRT1 Pathway on Proliferation of Gastric Cancer Cells

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作  者:任春梅[1] 许斌[1] 文黎明[1] 李林艳[1] 薛丽蓉 REN Chun-mei;XU Bin;WEN Li-ming;LI Lin-yan;XUE Li-rong(Sichuan Mianyang 404 Hospital,Mianyang 621000,China)

机构地区:[1]四川绵阳四〇四医院,四川绵阳621000

出  处:《肿瘤学杂志》2020年第9期791-795,共5页Journal of Chinese Oncology

基  金:四川省卫生厅科学研究项目(No16PJ376)。

摘  要:[目的]探讨miR-451靶向调控SIRT1通路对胃癌细胞增殖的作用机制研究。[方法]通过转染胃癌HepG2细胞实验进行分组,胃癌组、模拟物组和抑制物组,采用RT-PCR法检测HepG2细胞中miR-451、SIRT1 mRNA表达,流式细胞术检测HepG2细胞凋亡,Western blot检测细胞中SIRT1蛋白水平,细胞克隆测定细胞存活率,裸鼠皮下成瘤实验检测小鼠肿瘤体积。[结果]模拟物组miR-451表达量高于其他两组,与抑制物组相比,胃癌组miR-451表达水平较高(t=8.651,P<0.001)。胃癌组SIRT1表达高于模拟物组,与抑制物组相比,胃癌组和模拟物组SIRT1表达水平明显降低(t=6.362,P<0.001),三组比较差异有显著性(F=3.565,P<0.001)。与胃癌组相比,模拟物组HepG2细胞凋亡明显增加,胃癌组和抑制物组细胞凋亡情况均弱于模拟物组,三组比较差异有显著性(χ2=9.797,P=0.007)。胃癌组和抑制物组HepG2细胞单克隆形成率有上升趋势,模拟物组明显下降,三组比较组间差异有显著性(F=6.031,P<0.001)。模拟物组小鼠肿瘤体积较抑制物组明显变小,与胃癌组相比,抑制物组肿瘤体积增加,三组比较差异有显著性(F=9.967,P<0.001)。[结论] miR-451过表达可以抑制SIRT1通路相关蛋白活性,促进胃癌HepG2细胞凋亡,抑制其增殖和发展。[Objective] To investigate the mechanism of miR-451 targeting and regulating the proliferation of gastric cancer cells by SIRT1 pathway. [Methods] Grouped by transfection of gastric cancer Hep G2 cells,gastric cancer group,mimic group,inhibitor group. The expression of miR-451 and SIRT1 m RNA in Hep G2 cells was detected by RT-PCR. Conditions,flow cytometry was used to detect the apoptosis of Hep G2 cells,Western blot was used to detect the level of SIRT1 protein,cell clones were used to determine the cell survival rate,and subcutaneous tumor formation experiments in nude mice were used to detect the tumor volume in mice. [Results]The miR-451 expression level in the mimic group was higher than other targets,and the miR-451 expression level was higher in the inhibitor group(t=8.651,P<0.001),the expression of SIRT1 in the gastric cancer group was higher than that in the mimic group and the ratio of the inhibitor group,the expression level of SIRT1 in gastric cancer group and simulant group was significantly reduced(t=6.362, P<0.001),and the difference between the three groups was significant(F=3.565,P<0.001). The Hep G2 cells in the control group increased significantly,and the cellular resistance of the gastric cancer group and the inhibitor group were weaker than those in the mimic group.The three groups were significantly different(χ2=9.797,P =0.007). The tumor formation rate of Hep G2 cells in the gastric cancer group and the inhibitor group had an upward trend,the simulant group decreased significantly,and the difference between the three groups was significant(F=6.031,P<0.001). The tumor volume of mice in the mimic group was significantly smaller than that in the inhibitor group. Compared with the gastric cancer group,the tumor volume increase in the inhibitor group was significantly different among the three groups(F=9.967,P<0.001). [Conclusion] Overexpression of miR-451 can inhibit the activity of SIRT1 pathway-related proteins,promote the apoptosis of Hep G2 cells,and inhibit its proliferation and develop

关 键 词:HEPG2细胞 SIRT1通路 miR-451 胃癌 

分 类 号:R735.2[医药卫生—肿瘤]

 

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