Long Non-Coding RNA B3GALT5-AS1 Suppresses Keloid Progression by Regulating the β-Trcp1-Mediated Ubiquitination of

Wei Ye1, Junwen Lu1, Zuxian Yang2

  • 1Department of Burn Surgery, the First Clinical Medical College of Guangdong Medical University, Huizhou, 516001, People's Republic of China.

Abstract

Insights

Long non-coding RNA B3GALT5-AS1 inhibits keloid formation by downregulating HuR stability and glycolysis. This study identifies B3GALT5-AS1 as a potential therapeutic target for keloid treatment.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Oncology

Background:

  • The role of long non-coding RNA B3GALT5-AS1 in keloid progression is unknown.
  • B3GALT5-AS1 is implicated in colon and gastric cancers.

Purpose of the Study:

  • Investigate the molecular mechanisms of B3GALT5-AS1 in keloid fibroblast proliferation and invasion.
  • Determine the regulatory role of B3GALT5-AS1 in keloid formation.

Main Methods:

  • Analyzed lncRNA sequencing data (GSE158395) to identify differentially expressed lncRNAs.
  • Performed cell proliferation, migration, invasion, and glycolysis assays.
  • Utilized RNA pull-down, immunoprecipitation, ubiquitination, and rescue experiments to elucidate molecular interactions.

Main Results:

  • B3GALT5-AS1 was significantly downregulated in keloid tissues.
  • Overexpression of B3GALT5-AS1 inhibited keloid fibroblast proliferation, glycolysis, invasion, and migration.
  • B3GALT5-AS1 reduced HuR stability via β-Trcp1-mediated ubiquitination, and HuR overexpression reversed B3GALT5-AS1's inhibitory effects.

Conclusions:

  • B3GALT5-AS1 inhibits keloid formation by targeting the HuR/glycolysis pathway.
  • B3GALT5-AS1 represents a potential therapeutic target for keloid treatment.

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