Identification of the /miR-106a-5p/ZNF148 feedback loop in regulating HaCaT cell proliferation, migration and apoptosis.

This study aims to investigate the function of positive feedback loops involving noncoding RNA in diabetic wound healing. We developed a mouse diabetic wound model to confirm that hyperglycemia can impair wound healing. We also used an keratinocyte model in high-glucose conditions to investigate the mechanism of delayed wound healing. was decreased in diabetic mouse wound tissue and can promote keratinocyte biological functions. could bind to miR-106a-5p to modulate the expression of , a target gene of miR-106a-5p. Surprisingly, ZNF148 bound to a region in the promoter to stimulate gene expression. ZNF148-activated increases expression by competitively binding miR-106a-3p, generating a positive feedback loop that enhances keratinocyte function.