Abstract
Keloid is characterized by hyper-proliferation of fibroblasts and excess extracellular matrix (ECM) deposition. Transmembrane protein 88 (TMEM88), belonging to the TMEM family, was involved in the regulation of tumorigenesis and fibrogenesis. However, the role of TMEM88 in keloid formation remains unclear. This study aimed to investigate the effects of TMEM88 on keloid-derived fibroblasts (KFs) proliferation and ECM expression, and explore the underlying mechanism. Our results demonstrated that TMEM88 was lowly expressed in human keloid tissues and TGF-β1-stimulated KFs. TMEM88 overexpression significantly inhibited the proliferation and migration of KFs, as well as suppressed ECM expression in TGF-β1-stimulated KFs. Furthermore, TMEM88 overexpression greatly inhibited the protein levels of β-catenin, cyclin D1 and c-myc in TGF-β1-stimulated KFs. In conclusion, our data indicate that TMEM88 inhibits the TGF-β1-stimulated cell proliferation, migration and ECM expression in KFs through the inactivation of Wnt/β-catenin signaling pathway. Therefore, TMEM88 may be a potential therapeutic target for treating keloids.
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