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作 者:利民 韩思源 李苏明 郑超 舒苗江 龚祖元 张涛 杨森 LI Min;HAN Siyuan;LI Suming;ZHENG Chao;SHU Miaojiang;GONG Zuyuan;ZHANG Tao;YANG Sen(Department of Hepatobiliary Surgery,Dongguan Songshanhu Central Hospital,Dongguan,Guangdong,523326,China;Department of Infectious Disease,Dongguan Songshanhu Central Hospital,Dongguan,Guangdong,523326,China)
机构地区:[1]东莞市松山湖中心医院肝胆外科,广东省东莞市523326 [2]东莞市松山湖中心医院感染科,广东省东莞市523326
出 处:《医学分子生物学杂志》2023年第2期135-140,共6页Journal of Medical Molecular Biology
基 金:东莞市卫生和计划生育局科技计划项目(No.201950715024201)。
摘 要:目的分析miR-3682-3p与PI3K/AKT信号通路在肝细胞癌发展中的关系,以期为肝细胞癌的治疗提供新的思路。方法通过qRT-PCR分析MIHA人正常肝细胞和SMMC-7721人肝癌细胞中miR-3682-3p与PI3K/AKT的表达水平。通过转染不同质粒将SMMC-7721人肝癌细胞分为miR-3682-3p mimic组、miR-3682-3p mimic NC组、miR-3682-3p inhibitor组和miR-3682-3p inhibitor NC组,采用双荧光素酶报告基因实验分析miR-3682-3p与PI3K的相互作用关系。采用蛋白免疫印迹、qRT-PCR、流式细胞术、细胞划痕和Transwell实验分析不同实验组细胞的增殖、侵袭和凋亡情况。结果miR-3682-3p能够靶向调控PI3K/AKT信号通路,miR-3682-3p表达能够激活PI3K/AKT信号通路,肝癌细胞的增殖、迁移和侵袭能力增强,凋亡减少。而抑制miR-3682-3p表达后,PI3K/AKT通路受到抑制,肝癌细胞的增殖、迁移和侵袭能力减弱,凋亡增加。结论PI3K是miR-3682-3p的直接靶点,miR-3682-3p通过激活PI3K/AKT通路促进SMMC-7721人肝癌细胞的体外转移活性。Objective To analyze the relationship between miR-3682-3p and PI3K/AKT signaling pathway in the development of hepatocellular carcinoma,in order to provide new ideas for the treatment of hepatocellular carcinoma.Methods The expression levels of miR-3682-3p and PI3K/AKT in MIHA human normal hepatocytes and SMMC-7721 human hepatoma cells were detected by qRT-PCR.SMMC-7721 human hepatoma cells were divided into miR-3682-3p mimic group,miR-3682-3p mimic NC group,miR-3682-3p inhibitor group and miR-3682-3p inhibitor NC group by transfection of different plasmids.The interaction between miR-3682-3p and PI3K was analyzed by dual-luciferase gene reporter assay.Western blotting,qRT-PCR,flow cytometry,wound healing assay and transwell assay were used to analyze the proliferation,invasion and apoptosis of cells in different groups.Results miR-3682-3p could targetly regulate and activate the PI3K/AKT signaling pathway,and enhance the proliferation,migration and invasion of hepatoma cells,reduce the apoptosis.When the expression of miR-3682-3p was inhibited,the PI3K/AKT pathway was suppressed,the proliferation,migration and invasion of hepatoma cells were decresed,and the apoptosis was increased.Conclusion PI3K is a target of miR-3682-3p,and miR-3682-3p promotes the in vitro metastatic activity of SMMC-7721 human hepatoma cells by activating the PI3K/AKT pathway.
关 键 词:miR-3682-3p PI3K/AKT SMMC-7721 肝癌
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