LncRNA linc00312 regulates postoperative scar formation by adjusting miR-9

Abstract Background: Postoperative scar formation is a typical aspect of the physiological process of wound recovery, but issues with the healing process can lead to the formation of hypertrophic scar (HS). Objectives: To delved into the interaction between linc00312 and miR-9, and additionally analyzed their impacts on the growth and apoptosis of HS fibroblasts. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to determine the expression levels of linc00312 and miR-9, cell viability of scar fibroblasts was measured by cell counting kit-8 (CCK-8), flow cytometry was employed to determine the apoptosis rate of cells, cell clone formation assay was used to determine the proliferative capacity of cells, and the targeted regulation of linc00312 on miR-9 was validated through dual luciferase reporter gene experiments. The biological processes and molecular mechanisms of scar formation are studied through gene ontology and kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis. Results: The expression of linc00312 was noticeably enhanced in scar tissue, in contrast to the significantly diminished expression of miR-9, suggesting an inverse correlation between the two. Linc00312 stimulated the proliferation of HS fibroblasts and prevented their apoptosis rate, while miR-9 displayed the opposite effect. Linc00312 governs the activities of HS fibroblasts through the manipulation of miR-9. Conclusion: Long noncoding RNA (LncRNA) linc00312 regulates postoperative scar formation through miR-9 mediation. LncRNA linc00312/miR-9 could potentially serve as therapeutic targets for addressing postoperative scarring.