| Literature DB >> 31430452 |
Rui Wang1, Zhuanli Bai1, Xiulin Wen1, Huicong Du1, Lin Zhou1, Zhishui Tang1, Zhuangqun Yang2, Wei Ma3.
Abstract
Emerging evidence has revealed that microRNAs (miRNAs) play critical roles in keloid pathogenesis. However, potential molecular mechanism of keloid formation remains unclear. In the present study, our findings showed that miR-152-3p mRNA expression level was notably up-regulated in keloid tissues and keloid fibroblasts compared with that of normal skin tissues and normal skin fibroblasts, respectively. Furthermore, miR-152-3p inhibition remarkably suppressed cell proliferation, which was increased by miR-152-3p overexpression. Cell invasion was also significantly decreased by miR-152-3p inhibition, whereas was increased by miR-152-3p overexpression. The mRNA and protein expression levels of extracellular matrix components including type I collagen, type III collagen and fibronectin were decreased by miR-152-3p inhibition, but were increased by miR-152-3p overexpression. In addition, results of dual-luciferase reporter assay indicated that FOXF1 is a direct target of miR-152-3p. FOXF1 overexpression significantly inhibits cell proliferation, invasion, and extracellular matrix in keloid fibroblasts, and the suppressive effects of miR-152-3p mimic on these functions were notably partly reversed by FOXF1 overexpression. Taken together, these findings indicated that miR-152-3p regulates cell proliferation, invasion and extracellular matrix expression through targeting FOXF1 in keloid fibroblasts, suggesting that miR-152-3p is a novel and promising molecular target for keloid treatment.Entities:
Keywords: Cell proliferation; Extracellular matrix; FOXF1; Invasion; Keloid fibroblasts; miR-152-3p
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Year: 2019 PMID: 31430452 DOI: 10.1016/j.lfs.2019.116779
Source DB: PubMed Journal: Life Sci ISSN: 0024-3205 Impact factor: 5.037