Lncrna Col1a2-As1 Promotes Skin Fibroblast Apoptosis By Repressing P-Smad3 And Promoting Beta-Catenin Expression

LncRNA COL1A2-AS1 has been demonstrated to inhibit fibroblast proliferation of hypertrophic scars. However, the function of COL1A2-AS1 in normal skin fibroblasts remains poorly studied. Here, we report that overexpression of COL1A2-AS1 promoted normal skin fibroblast apoptosis. On the basis of mRNA-seq data and gene set enrichment analysis plus Kyoto encyclopedia of genes and genomes pathway analysis, 16 upregulated and 125 downregulated mRNAs were found; TGF-beta, Wnt, and MAPK pathways were potentially involved. Western blot assay confirmed that overexpression of COL1A2-AS1 repressed p-Smad3 expression and promoted beta-catenin expression. Furthermore, COL1A2-AS1 overexpression combined with either TGF-beta 1 or siRNA against beta-catenin reversed the upregulation of apoptosis in the COL1A2-AS1 overexpression group. In conclusion, our study revealed the roles of COL1A2-AS1 in normal skin fibroblast apoptosis, with COL1A2-AS1 functioning by repressing p-Smad3 expression and promoting beta-catenin expression.