Department of dermatology, the Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, Wuxi, China.
Int Wound J. 2023 May;20(5):1517-1524. doi: 10.1111/iwj.14006. Epub 2022 Nov 4.
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.
先前的研究表明,c-Myc 可能促进瘢痕疙瘩成纤维细胞的增殖和胶原积累。泛素特异性肽酶 37(USP37)介导的 c-Myc 去泛素化和稳定对于肺癌增殖至关重要,而 USP37 在瘢痕疙瘩成纤维细胞中的潜在作用尚未得到研究。通过 RT-PCR 或 ELISA 检测到瘢痕疙瘩组织中 USP37、c-Myc 和 Collagen I 含量升高。用 Lipofectamine 3000 将 USP37 过表达质粒或 USP37 短发夹 RNA(shRNA)转染到瘢痕疙瘩成纤维细胞中,以阐明 USP37 在瘢痕疙瘩成纤维细胞中的作用。USP37 过表达可促进瘢痕疙瘩成纤维细胞的增殖,增加 c-Myc 和 Collagen I 的表达。另一方面,USP37 shRNA 抑制了瘢痕疙瘩成纤维细胞的增殖,降低了 c-Myc 和 Collagen I 的表达。值得注意的是,C-Myc 过表达促进了 USP37 shRNA 抑制的瘢痕疙瘩成纤维细胞的增殖,同时 Collagen I 的表达增加。所有这些结果表明,USP37 可以通过调节 c-Myc 来促进瘢痕疙瘩成纤维细胞的增殖和胶原沉积,并且可以在未来的瘢痕疙瘩治疗中靶向 USP37。