医学分子生物学杂志 ›› 2023, Vol. 20 ›› Issue (2): 135-140.doi: 10.3870/j.issn.1672-8009.2023.02.006

• 论著 • 上一篇    下一篇

miR-3682-3p 通过调控 PI3K/ AKT 信号通路影响 SMMC-7721 人 肝癌细胞的增殖、 侵袭和凋亡

  

  1. 东莞市松山湖中心医院1肝胆外科, 2感染科 广东省东莞市, 523326
  • 出版日期:2023-03-31 发布日期:2023-05-23
  • 基金资助:
    东莞市卫生和计划生育局科技计划项目 (No. 201950715024201) 

Effect of miR-3682-3p on Proliferation, Invasion and Apoptosis of SMMC-7721 Human Hepatoma Cells by Regulating PI3K / AKT Signaling Pathway

  1. 1Department of Hepatobiliary Surgery, 2Department of Infectious Disease, Dongguan Songshanhu Central Hospital, Dongguan, Guangdong, 523326, China
  • Online:2023-03-31 Published:2023-05-23

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。

关键词: miR-3682-3p, PI3K/ AKT, SMMC-7721, 肝癌 

Abstract: 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.

Key words: miR-3682-3p, PI3K/ AKT, SMMC-7721, liver cancer 

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