Diabetology & Metabolic Syndrome · 10 authors, 2 centres
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This preclinical study used diabetic ulcer rat models and high glucose-induced human keratinocytes (HaCaT cells) to show that silencing the long noncoding RNA XIST inhibits cell proliferation and migration by increasing miR-126-3p, which targets and reduces EGFR expression, leading to delayed wound healing.
This preclinical study investigated the role of lncRNA XIST in diabetic foot ulcers (DFUs) using a rat model and a high glucose-induced HaCaT cell line. Researchers found that XIST and EGFR expression were downregulated, while miR-126-3p was upregulated in diabetic ulcer tissues and high glucose-treated cells. Molecular assays confirmed XIST binds to miR-126-3p, and miR-126-3p directly targets EGFR. Silencing XIST increased miR-126-3p and decreased EGFR, which inhibited the proliferation and migration of high glucose-treated HaCaT cells. These effects were reversed by a miR-126-3p inhibitor or EGFR overexpression. The study concludes that decreased XIST inhibits keratinocyte proliferation and migration via the miR-126-3p/EGFR axis, contributing to delayed wound healing in DFUs.
