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Updated: Jun 27, 2025

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
Published on: July 28, 2023
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.
Background:
lncRNA β‑1,3‑galactosyltransferase 5‑AS1 (B3GALT5-AS1) plays a vital regulatory role in colon and gastric cancers. However, the biological functions and regulatory mechanisms of B3GALT5-AS1 in keloid progression remain unknown. This study aims to investigate the molecular mechanisms in the B3GALT5-AS1-regulated keloid proliferation and invasion.
Methods:
Secondary mining of the lncRNA sequencing data from GSE158395 was conducted to screen differentially expressed lncRNAs between keloid and normal tissues. MTT, cell migration and invasion assays were performed to detect the effects of B3GALT5-AS1 on keloid fibroblasts (KFs) proliferation and metastasis. The extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were also determined to evaluate glycolysis in KFs. RNA pull-down and RNA-protein immunoprecipitation assays were used to confirm the interaction between B3GALT5-AS1 and Hu-Antigen R (HuR). Further ubiquitination and rescue experiments were performed to elucidate the regulatory relationship between B3GALT5-AS1 and HuR.
Results:
B3GALT5-AS1 was significantly down-regulated in keloid tissues and fibroblasts. B3GALT5-AS1 overexpression significantly inhibited KFs proliferation, glycolysis, invasion, and migration and promoted cell apoptosis, whereas silencing B3GALT5-AS1 inhibited these effects. Moreover, B3GALT5-AS1 binds to HuRand reduces its stability through β-Transducin repeats-containing protein 1 (β-Trcp1)-mediated ubiquitination. Overexpression of HuR reversed the inhibition of B3GALT5-AS1 on cell proliferation, migration, and invasion in KFs, where glycolysis pathway was involved.
Conclusion:
Our findings illustrate that B3GALT5-AS1 has great effect on inhibition of keloid formation, which provides a potential target for keloid therapy.
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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