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.

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.

Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.7K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.5K
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
7.4K