SDC1 Influences Keloid Fibroblasts Migration and Invasion via Targeting Wnt/β-Catenin Signaling Pathway Mediated EMT.

Abstract

Keloid is the result of abnormal wound healing, puzzled by the invasive growth and high recurrence rate attributed to its complex pathogenic mechanism. Syndecan1 (SDC1) contributes to regulating cell migration and invasion by activating epithelial-mesenchymal transition (EMT) in tumor and fibrotic disease. Herein, using western blot analysis, the authors assessed the role of SDC1 on EMT in keloid and its underlying mechanism. The authors found keloid fibroblasts exhibited a higher proportion of mesenchymal phenotypes, and SDC1 was significantly upregulated in keloid fibroblasts. Then, the authors transfected small interfering RNA targeting SDC1 in keloid fibroblasts and tested the abilities of cell migration and invasion, as well as the expression of EMT-related markers, including N-cadherin, vimentin, and E-cadherin. The results showed that the knockdown of SDC1 markedly suppressed the migration and invasion abilities of keloid fibroblasts and reduced the phenotypes of EMT by inhibiting Wnt/β-catenin signaling pathway. The authors' findings suggest that SDC1 may influences keloid fibroblasts migration and invasion through targeting Wnt/β-catenin signaling pathway mediated EMT, which supports its potential value as a therapeutic target for the treatment of keloid.