ArticleArchives of dermatological research2023
SNHG1 functions as a ceRNA in hypertrophic scar fibroblast proliferation and apoptosis through miR-320b/CTNNB1 axis.
Article in Archives of dermatological research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- LncRNA SNHG1 regulates human keratinocyte function by targeting miR-199a-3p to delay skin wound healing.Archives of dermatological research · 2025Article
- Multi-Omics Association Analysis of Mitochondrial Genes in Hypertrophic Scars: Application of Mendelian Randomization.Journal of inflammation research · 2025Article
- Urinary exosomal miR-320b as a biomarker of tubular atrophy/interstitial fibrosis in IgA nephropathy patients.American journal of translational research · 2025Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.