Silencing lncRNA XIST enhances MiR-146a-5p expression levels to promote cutaneous acute wound healing

Abstract Objectives Surgical skin wounds impair patient mobility and pose a risk of infection. Long non-coding RNA XIST shows abnormal expression in burned skin. This study explores its expression in acute wounds and its impact on wound healing (WH). Methods An in vitro skin injury model was established by treating human immortalized keratinocytes (HaCaT) cells with 6 μg/mL lipopolysaccharide (LPS). Cell proliferation, apoptosis, and migration were evaluated using cell counting kit-8 (CCK-8), flow cytometry, and Transwell assay, respectively. Binding sites between XIST and miR-146a-5p were predicted using the ENCORI database. Dual-luciferase reporter assays confirmed their interaction. XIST and miR-146a-5p levels were quantified via real-time quantitative reverse transcription PCR (RT-qPCR). Enzyme-linked immunosorbent assay (ELISA) assay was used to measure the levels of inflammatory and growth factors in cells. Results XIST was overexpressed in the skin acute wound model, whereas miR-146a-5p was at a low level in the wound model. XIST is bound directly to miR-146a-5p. Silencing XIST elevated miR-146a-5p levels. LPS treatment restored the proliferation and migration of damaged HaCaT cells, reduced apoptosis rates, decreased inflammatory factors levels, and increased growth factors levels. Conclusions XIST may be detrimental to WH. Knocking down XIST to enhance miR-146a-5p expression could boost HaCaT cells physiological activity, offering a potential therapeutic target for promoting WH.