Effect of RNF113A on the malignant biological behavior of hepatocellular carcinoma cells
10.3969/j.issn.1009-9905.2024.04.005
- VernacularTitle:RNF113A对肝细胞癌细胞恶性生物学行为的影响研究
- Author:
Hai-Jie DAI
1
,
2
;
Xia HUANG
;
Li-Jun DONG
;
Ming-Xuan XING
;
Teng-Yue ZOU
;
Wen-Xiao LI
Author Information
1. 滨州医学院(山东 烟台 264199)
2. 中国人民解放军联勤保障部队第九七○医院 普外科(山东 威海 264200)
- Keywords:
Hepatocellular carcinoma;
RNF113A;
AMPK;
Cell proliferation;
Cell invasion;
Cell migration;
Autophagy;
Apoptosis
- From:
Chinese Journal of Current Advances in General Surgery
2024;27(4):275-281
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effects of RNF113A on the proliferation,migration,in-vasion,apoptosis,and autophagy of hepatocellular carcinoma cells.Methods:Hep3B cells were divided into control group and RNF113A overexpression group(RNF113A-OE),HepG2 was divided into control group and RNF113A knockdown group(si-RNF113A),CCK-8 assay was used to detect changes in cell viability,clone formation assay was used to detect changes in cell proliferation abili-ty,Transwell assay was used to detect changes in cell invasion ability,wound healing assay was used to detect changes in cell migration ability,and flow cytometry was used to detect changes in cell apoptosis ability,Western blot experiments were used to detect changes in protein expression of autophagy related genes and AMPK signaling pathway related genes.Results:Compared with the control group,the proliferation,cloning,invasion,and migration abilities of Hep3B cells in the RNF113A-OE group were improved,while apoptosis and autophagy abilities were decreased,and the AMPK signaling pathway was inhibited;In the si-RNF113A group,the proliferation,cloning,in-vasion,and migration abilities of HepG2 cells were significantly reduced,while apoptosis and au-tophagy abilities were increased,and the activation of the AMPK signaling pathway was promoted.Conclusion:RNF113A promotes the proliferation,cloning,invasion,and migration of hepatocel-lular carcinoma cells,and inhibited apoptosis and autophagy by inhibiting the AMPK signaling path-way.
