SNHG1 functions as a ceRNA in hypertrophic scar fibroblast proliferation and apoptosis through miR-320b/CTNNB1 axis.

Abstract

Hypertrophic scar (HS) is a fibrotic disease caused by skin injury. Competing endogenous RNA (ceRNA) has been demonstrated to implicate in the regulation of cell malignant phenotypes. This research aims to reveal the effect of catenin beta 1 (CTNNB1) on the functions of hypertrophic scar fibroblasts (HSFBs) and its role in a ceRNA network. RNA expression level was assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). The proliferation and apoptosis of HSFB was detected via Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis. Mechanism experiments included RNA pull down assay, luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay were applied to analyze the upstream molecular mechanism of CTNNB1. CTNNB1 was highly expressed in HSFB. CTNNB1 depletion repressed malignant growth of HSFB. Mechanically, CTNNB1 was targeted by microRNA-320b (miR-320b) in HSFB. Small nucleolar RNA host gene 1 (SNHG1) aced as a ceRNA to upregulate CTNNB1 expression via sponging miR-320b in HSFB. CTNNB1 overexpression could reverse the impact of SNHG1 depletion on the proliferation and apoptosis of HSFB. SNHG1 acts as a ceRNA in modulating HSFB proliferation and apoptosis through miR-320b/CTNNB1 axis. SNHG1 act as a ceRNA to promote HSFB growth by sponging miR-320b to upregulate CTNNB1.