Microrna-342 inhibits hepatocellular carcinoma cell proliferation and promotes apoptosis through the FOXP1/MYCBP Signaling Axis.

IF 2.2 4区 医学 Q3 TOXICOLOGY
Toxicology Research Pub Date : 2024-12-17 eCollection Date: 2024-12-01 DOI:10.1093/toxres/tfae149
Yanling Zhang, Guang Da Yang, Qian Ya Chen, Jinlong Zeng, Yang Cao
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引用次数: 0

Abstract

To investigate the role and mechanism of miR-342 and FOXP1 on hepatocellular carcinoma cells. QRT-PCR was applied to determine the expression of miR-342, FOXP1 and MYCBP in normal hepatocyte cell lines (NHC), hepatocellular carcinoma cell lines (HEK-293 T) and human hepatocellular carcinoma cell lines (HepG2, MHCC97-L, Huh7 and SMMC7721). After knockdown or over-expression of miR-342 and FOXP1 in HepG2 cells respectively, cell proliferation and cell viability were measured using MTT assay and colony formation assay. Flow cytometry was adopted to test for apoptosis. Dual luciferase gene reporter assays were performed to validate the target relationship between FOXP1and miR-342 or MYCBP. The level of apoptosis-related proteins cleaved-caspase-3, Bcl-2 and Bax were measured by western blot. Compared with NHC, miR-342 expression was decreased and FOXP1 expression was up-regulated in hepatocellular carcinoma cell lines. MiR-342 could target and negatively regulate FOXP1. FOXP1 could promote the proliferation of hepatocellular carcinoma cells, positively regulate the expression of c-Caspase-3, Bax, negatively regulate Bcl-2 and inhibit apoptosis. FOXP1 can also target and positively regulate MYCBP. The expression of MYCBP was up-regulated in the hepatocellular carcinoma cell lines, while overexpression of miR-342 decreased MYCBP expression promoted by overexpression of FOXP1. MiR-342 can inhibit FOXP1/MYCBP signaling axis to regulate the members of Caspase-3 and Bcl-2 family to inhibit the proliferation and promote apoptosis of hepatocellular carcinoma cells.

Microrna-342通过FOXP1/MYCBP信号轴抑制肝癌细胞增殖并促进细胞凋亡。
探讨miR-342和FOXP1在肝癌细胞中的作用及机制。采用QRT-PCR检测miR-342、FOXP1和MYCBP在正常肝细胞系(NHC)、肝癌细胞系(HEK-293 T)和人肝癌细胞系(HepG2、MHCC97-L、Huh7和SMMC7721)中的表达情况。在HepG2细胞中分别敲低或过表达miR-342和FOXP1后,采用MTT法和集落形成法检测细胞增殖和细胞活力。采用流式细胞术检测细胞凋亡。采用双荧光素酶基因报告试验来验证foxp1与miR-342或MYCBP之间的靶标关系。western blot检测凋亡相关蛋白caspase-3、Bcl-2、Bax的表达水平。与NHC相比,肝癌细胞系中miR-342表达降低,FOXP1表达上调。MiR-342可以靶向并负向调控FOXP1。FOXP1能够促进肝癌细胞的增殖,正调控c-Caspase-3、Bax的表达,负调控Bcl-2的表达,抑制细胞凋亡。FOXP1也可以靶向MYCBP并积极调节。肝癌细胞系中MYCBP的表达上调,而过表达miR-342降低了FOXP1过表达促进的MYCBP表达。MiR-342可抑制FOXP1/MYCBP信号轴调控Caspase-3和Bcl-2家族成员,抑制肝癌细胞增殖,促进细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Toxicology Research
Toxicology Research TOXICOLOGY-
CiteScore
3.60
自引率
0.00%
发文量
82
期刊介绍: A multi-disciplinary journal covering the best research in both fundamental and applied aspects of toxicology
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