Low LINC01189 targets miR-564 to promote fibroblast proliferation and extracellular matrix deposition, thereby exacerbating scar formation

To preliminarily elucidate the diagnostic mechanism of long intergenic noncoding RNA 01189 (LINC01189) in burn scar patients and its regulatory role in scar formation. A total of 115 burn scar patients and 98 healthy individuals were enrolled. Patient tissue was obtained via scar excision or skin grafting. Logistic regression analyzed risk factors for scar formation, whilst receiver operating characteristic (ROC) curves assessed the diagnostic value of LncRNA for burn scar patients. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) measured gene expression; cell counting kit-8 (CCK-8) and Transwell assays assessed cell proliferation and migration; flow cytometry recorded apoptosis. Dual luciferase reporter assays and RNA immunoprecipitation validated gene–gene interactions. LINC01189 was downregulated in serum and skin tissue from burn scar patients, acting as a protective factor against scar formation. LINC01189 shows promising diagnostic potential for burn scar patients. Transfection with oe-LINC01189 inhibited the proliferation and migration of human keloid-derived fibroblasts (HKFs), suppressed the extracellular matrix (ECM) synthesis gene expression, and promoted apoptosis. miR-564 is a target gene of LINC01189, exhibiting a negative correlation with it, and is upregulated in burn scar patients and HKFs. Transfection of a miR mimic counteracts the cellular functional and gene expression alterations induced by LINC01189 overexpression. LINC01189 acts as a protective factor against scar formation. Its downregulation promotes HKFs proliferation and migration via miR-564, increases ECM accumulation, and exacerbates scarring.