The deubiquitinating enzyme USP37 promotes keloid fibroblasts proliferation and collagen production by regulating the c‐Myc expression. Issue 5 (4th November 2022)

• Record Type: Journal Article
• Authors: Piao, Meishan; Feng, Guangdong
• Is Part Of: International wound journal. Volume 20:Issue 5(2023)
• Page Start: 1517
• Page End: 1524
• Publication Date: 2022-11-04
• Subjects: c‐Myc -- collagen I -- fibroblasts -- keloid -- USP37; Wounds and injuries -- Treatment -- Periodicals; Wounds and injuries -- Periodicals; Wound healing -- Periodicals; 617.1005
• DOI: 10.1111/iwj.14006
• Languages: English
• ISSNs: 1742-4801

Abstract

Abstract: Previous research testifies that c‐Myc may promote keloid fibroblast proliferation and collagen accumulation. Ubiquitin‐specific peptidase 37 (USP37)‐mediated deubiquitination and stabilisation of c‐Myc are vital for lung cancer proliferation, while the potential role of USP37 in keloid fibroblasts is not investigated. Elevated USP37, c‐Myc, and Collagen I content were detected in keloid tissue with RT‐PCR or ELISA assay. USP37 over‐expression plasmids or USP37 short hairpin RNAs (shRNAs) were transfected into keloid fibroblasts with Lipofectamine 3000 to decipher the role of USP37 in keloid fibroblasts. USP37 overexpression could promote the proliferation of keloid fibroblasts with increased c‐Myc and Collagen I expression. On the other hand, USP37 shRNAs inhibited the proliferation of keloid fibroblasts with diminished c‐Myc and Collagen I expression. It was worth noting that C‐Myc overexpression promoted the proliferation of keloid fibroblasts inhibited by USP37 shRNAs with increasing Collagen I expression. All of these results demonstrate that USP37 could regulate c‐Myc to promote the proliferation and collagen deposit of keloid fibroblasts, and USP37 could be targeted in future keloid therapy.