|本期目录/Table of Contents|

[1]全养雅,黎慧娟,陈仕,等.miR-5188在肝癌细胞中的作用及网络调控机制研究[J].国际消化病杂志,2023,06:394-400.
 QUAN Yangya,LI Huijuan,CHEN Shi,et al.Role of miR-5188 in liver cancer cells and its network regulation mechanism[J].International Journal of Digestive Disease,2023,06:394-400.
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miR-5188在肝癌细胞中的作用及网络调控机制研究(PDF)

《国际消化病杂志》[ISSN:1673-534X/CN:31-1953/R]

期数:
2023年06期
页码:
394-400
栏目:
论著
出版日期:
2023-12-30

文章信息/Info

Title:
Role of miR-5188 in liver cancer cells and its network regulation mechanism
作者:
全养雅黎慧娟陈仕周艳
410007 湖南长沙,湖南省脑科医院消化内科
Author(s):
QUAN Yangya LI Huijuan CHEN Shi ZHOU Yan.
Department of Gastroenterology, Hunan Provincial Brain Hospital, Changsha 410007, China
关键词:
miR-5188 肝细胞癌DIDO1 NEAT1 pri-miRNA
Keywords:
miR-5188 Hepatocellular carcinoma DIDO1 NEAT1 pri-miRNA
分类号:
-
DOI:
10.3969/j.issn.1673-534X.2022.06.008
文献标识码:
-
摘要:
目的探究miR-5188在肝癌细胞中的作用及网络调控机制。方法过表达或敲低miR-5188表达后,检测肝癌细胞HepG2的增殖能力。利用miRNA靶基因预测数据库miRDB获取miR-5188潜在的靶基因,使用小干扰RNA(siRNA)敲低HepG2细胞中的上述靶基因后检测细胞增殖能力。采用实时荧光定量PCR法检测正常肝细胞LO2和HepG2细胞中miR-5188、pre-miR-5188和pri-miR-5188的表达水平,并分析长链非编码RNANEAT1(下文简称NEAT1)、NONO/PSF复合体对pri-miR-5188的影响。结果过表达miR-5188后,HepG2细胞的增殖能力增强;敲低miR-5188表达后,HepG2细胞的增殖能力减弱,差异均有统计学意义(P均<0.05)。敲低DIDO1表达后,HepG2细胞的增殖能力增强;过表达DIDO1后,HepG2细胞的增殖能力减弱,差异均有统计学意义(P均<0.05)。过表达miR-5188后,HepG2细胞中DIDO1的表达水平降低;敲低miR-5188表达后,HepG2细胞中DIDO1的表达水平升高,差异均有统计学意义(P均<0.05)。双荧光素酶报告基因实验检测结果显示,miR-5188靶向DIDO1mRNA的3'非翻译区(3'-UTR)。与LO2细胞相比,HepG2细胞中miR-5188和pre-miR-5188的表达水平均显著升高,而pri-miR-5188的表达水平显著降低,差异均有统计学意义(P均<0.05)。与LO2细胞相比,HepG2细胞中NEAT1的表达水平显著升高(P<0.05),而NONO和PSF的表达水平差异均无统计学意义(P均>0.05)。敲低NEAT1、NONO或PSF表达后,HepG2细胞中pri-miR-5188的表达水平均显著升高(P均<0.05)。敲除NEAT1后,HepG2细胞中pri-miR-5188的表达水平升高,NONO与PSF的相互作用减弱,并且NONO/PSF与pri-miR-5188的结合减少。结论HepG2细胞中NEAT1的表达水平升高,提高了NONO/PSF复合体对pri-miR-5188的加工水平,增强了miR-5188/DIDO1轴对HepG2细胞增殖能力的正向作用。
Abstract:
Objective This paper is to investigate the role of miR-5188 in liver cancer cells and its network regulation mechanism. Methods? After overexpression or knockdown of miR-5188, the proliferation ability of HepG2 cell was detected. The potential target genes of miR-5188 were obtained using miRNA target gene prediction database miRDB, and the proliferation ability of HepG2 cells was detected after the above genes were knocked down using small interfering RNA (siRNA). Real-time fluorescence quantitative PCR was used to detect the expression of miR-5188, pre-miR-5188, and pri-miR-5188 in LO2 cells and HepG2 cells. The effects of long noncoding RNA NEAT1 (hereinafter referred to as NEAT1) and NONO/PSF complex on pri-miR-5188 were analyzed. Results? After overexpression of miR-5188, the proliferation ability of HepG2 cells is increased, and after knockdown of miR-5188, the proliferation ability of HepG2 cells is decreased, with statistically significant differences (P<0.05). After knockdown of DIDO1, the proliferation ability of HepG2 cells is increased, and after overexpression of DIDO1, the proliferation ability of HepG2 cells is decreased, with statistically significant differences (P<0.05). After overexpression of miR-5188, the expression of DIDO1 in HepG2 cells is decreased, and after knockdown of miR-5188, the expression of DIDO1 in HepG2 cells is increased, with statistically significant differences (P<0.05). The double luciferase reporter gene test results show that miR-5188 targets the 3' untranslated region (3'-UTR) of DIDO1 mRNA. Compared with LO2 cells, the expression of miR-5188 and pre-miR-5188 in HepG2 cells are increased, while the expression of pri-miR-5188 is decreased, with statistically significant differences (P<0.05). Compared with LO2 cells, the expression of NEAT1 in HepG2 cells is increased (P<0.05), while the expression of proteins NONO and PSF do not change (P>0.05). After knockdown of NEAT1, NONO or PSF, the expression of pri-miR-5188 in HepG2 cells is significantly increased (P<0.05). After knockout of NEAT1, the expression of pri-miR-5188 in HepG2 cells is increased, and the interaction between NONO and PSF is weakened, while the binding of NONO/PSF and pri-miR-5188 is decreased. Conclusion? The expression of NEAT1 is increased in HepG2 cells, which increases the processing of pri-miR-5188 by NONO/PSF complex, and enhances the positive effect of miR-5188/DIDO1 axis on the proliferation ability of liver cancer cells.

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备注/Memo

备注/Memo:
基金项目:湖南省卫计委科研计划项目(B20180176)
更新日期/Last Update: 1900-01-01