MiR-671-5p Promotes Cell Proliferation, Invasion, and Migration in Hepatocellular Carcinoma through Targeting ALDH2.

Abstract

We explored the mechanism of acetaldehyde dehydrogenase 2 (ALDH2) in modulating cell behaviors in hepatocellular carcinoma (HCC), and provided fresh ideas for targeted treatment of HCC. The target messenger RNA (mRNA) was determined by The Cancer Genome Atlas (TCGA) analysis, and the upstream regulatory gene miRNA was obtained by further analysis. The expression of ALDH2 mRNA and miR-671-5p in HCC cell lines was assayed by quantitative reverse transcription polymerase chain reaction (qRT-PCR), and protein expression was assessed by Western blot. The impact of ALDH2 on biological functions of HCC cells was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), wound-healing, and Transwell assays. Bioinformatics method was utilized to predict binding site of miR-671-5p and ALDH2, and their targeted relationship was detected by dual-luciferase gene assay, qRT-PCR and Western blot. ALDH2 expression was reduced in HCC tissue and cell lines. ALDH2 worked as a tumor inhibitor in HCC. Overexpressing ALDH2 could hinder proliferation, migration and invasion of HCC cells. miR-671-5p was the upstream regulatory gene of ALDH2, and it presented remarkably high expression in HCC. A negative modulatory relationship existed between miR-671-5p and ALDH2. The rescue experiments further illustrated the effects of the two on the malignant behaviors of HCC cells. Forced expression of miR-671-5p fostered the proliferation, migration and invasion of HCC cells by restraining ALDH2.