LncRNA COL1A2-AS1 promotes skin fibroblast apoptosis by repressing p-Smad3 and promoting β-catenin expression.
Jun LiYanli GaoQian LiLing ChenYajun ChenJingyun LiPublished in: Experimental dermatology (2021)
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-β, Wnt, and MAPK pathways were potentially involved. Western blot assay confirmed that overexpression of COL1A2-AS1 repressed p-Smad3 expression and promoted β-catenin expression. Furthermore, COL1A2-AS1 overexpression combined with either TGF-β1 or siRNA against β-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 β-catenin expression.
Keyphrases
- cell proliferation
- poor prognosis
- epithelial mesenchymal transition
- transforming growth factor
- oxidative stress
- wound healing
- endoplasmic reticulum stress
- long non coding rna
- signaling pathway
- cell cycle arrest
- binding protein
- genome wide
- transcription factor
- stem cells
- machine learning
- south africa
- big data
- electronic health record
- artificial intelligence