miR‑375 affects the hedgehog signaling pathway by downregulating RAC1 to inhibit hepatic stellate cell viability and epithelial‑mesenchymal transition.

Abstract:

:MicroRNAs (miRNAs/miRs) are a class of non‑coding RNAs that serve crucial roles in liver cancer and other liver injury diseases. However, the expression profile and mechanisms underlying miRNAs in liver fibrosis are not completely understood. The present study identified the novel miR‑375/Rac family small GTPase 1 (RAC1) regulatory axis in liver fibrosis. Reverse transcription‑quantitative PCR was performed to detect miR‑375 expression levels. MTT, flow cytometry and western blotting were performed to explore the in vitro roles of miR‑375. The dual‑luciferase reporter gene assay was performed to determine the potential mechanism underlying miR‑375 in liver fibrosis. miR‑375 expression was significantly downregulated in liver fibrosis tissues and cells compared with healthy control tissues and hepatocytes, respectively. Compared with the pre‑negative control group, miR‑375 overexpression inhibited mouse hepatic stellate cell (HSC) viability and epithelial‑mesenchymal transition, and alleviated liver fibrosis. The dual‑luciferase reporter assay results demonstrated that miR‑375 bound to RAC1. Moreover, the results indicated that miR‑375 regulated the hedgehog signaling pathway via RAC1 to restrain HSC viability and EMT, thus exerting its anti‑liver fibrosis function. The present study identified the miR‑375/RAC1 axis as a novel regulatory axis associated with the development of liver fibrosis.

journal_name

Mol Med Rep

authors

Liang Z,Li J,Zhao L,Deng Y

doi

10.3892/mmr.2020.11821

subject

Has Abstract

pub_date

2021-03-01 00:00:00

issue

3

eissn

1791-2997

issn

1791-3004

pii

182

journal_volume

23

pub_type

杂志文章