ArticleArchives of dermatological research2025
ERG transcriptionally activates SFRP1 to promote apoptosis of keloid fibroblasts and inhibit epithelial-mesenchymal transition and fibrosis through the Wnt3a/β-catenin pathway.
Article in Archives of dermatological research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Metabolic reprogramming and ferroptosis in keloid pathogenesis: new insights for targeted therapy.Molecular biology reports · 2026Review
- Epithelial-mesenchymal transition in cutaneous fibrosis disease: from mechanisms to therapy.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloids are benign skin tumors characterized by excessive fibrosis. Secreted frizzled-related protein 1 (SFRP1) has been linked to fibrosis regulation. Understanding SFRP1's role in keloid fibroblasts (KFs) could provide insights into the molecular mechanisms driving keloid progression and offer new therapeutic avenues. mRNA expression of SFRP1 and ETS-related gene 1 (ERG) was assessed via quantitative real-time polymerase chain reaction. Protein levels were determined by Western blotting. Cell viability was evaluated using cell counting kit-8 assay. Cell apoptosis was detected by flow cytometry. Cell invasion was assessed by transwell assay, and cell migration by wound-healing assay. Chromatin immunoprecipitation and dual-luciferase reporter assays were performed to elucidate the interaction of ERG and SFRP1. SFRP1 was downregulated in keloid tissues and KFs. Overexpression of SFRP1 induced KF apoptosis and inhibited epithelial-mesenchymal transition and fibrosis, concurrent with inactivation of the Wnt3a/β-catenin pathway. ERG was found to transcriptionally activate SFRP1. ERG overexpression promoted KF apoptosis and inhibited epithelial-mesenchymal transition and fibrosis by regulating SFRP1. Wnt3a/β-catenin pathway inactivation. Moreover, the inhibitory effects of ERG overexpression on the protein expression of Wnt3a and β-catenin were attenuated after SFRP1 knockdown. ERG's transcriptional activation of SFRP1 promoted KF apoptosis and inhibited epithelial-mesenchymal transition and fibrosis through the Wnt3a/β-catenin pathway, highlighting a potential therapeutic strategy for keloid management.
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Registered trials
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