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Updated: Aug 11, 2025

In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
Published on: May 1, 2020
SNHG1 functions as a ceRNA in hypertrophic scar fibroblast proliferation and apoptosis through miR-320b/CTNNB1 axis
Qiaoling Li1, Bowei Zhang2, Jie Lu3
1Center of Medical Cosmetology, Chengdu Second People's Hospital, No. 10, Qingyun South Street, Jinjiang District, Chengdu, 610011, Sichuan, China. liqiaoling1005@126.com.
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.
Insights
Small nucleolar RNA host gene 1 (SNHG1) promotes hypertrophic scar fibroblast growth by upregulating catenin beta 1 (CTNNB1) via the microRNA-320b (miR-320b) pathway. This ceRNA network impacts fibroblast proliferation and apoptosis.
Area of Science:
- Fibrotic disease research
- Molecular biology
- RNA regulation
Background:
- Hypertrophic scarring (HS) is a fibrotic skin condition.
- Competing endogenous RNA (ceRNA) networks regulate cell phenotypes.
- The role of catenin beta 1 (CTNNB1) in HS requires elucidation.
Purpose of the Study:
- Investigate CTNNB1's effect on hypertrophic scar fibroblasts (HSFBs).
- Determine CTNNB1's function within a ceRNA network.
- Elucidate the SNHG1/miR-320b/CTNNB1 axis in HS.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (RT-qPCR) for RNA expression.
- Cell Counting Kit-8 (CCK-8) assay and flow cytometry for proliferation and apoptosis.
- RNA pull down, luciferase reporter, and RNA-binding protein immunoprecipitation (RIP) assays for mechanism analysis.
Main Results:
- CTNNB1 expression was elevated in HSFBs.
- CTNNB1 depletion inhibited HSFB proliferation and promoted apoptosis.
- SNHG1 acted as a ceRNA, upregulating CTNNB1 by sponging miR-320b.
- CTNNB1 overexpression reversed SNHG1 depletion effects.
Conclusions:
- SNHG1 promotes HS by regulating HSFB proliferation and apoptosis via the miR-320b/CTNNB1 axis.
- The SNHG1/miR-320b/CTNNB1 ceRNA network is a key player in hypertrophic scar formation.
- Targeting this pathway may offer therapeutic strategies for hypertrophic scars.
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