Long non-coding RNA LINC01315 accelerates the development of endometriosis through the miR-497-5p/BDNF axis

Endometriosis (EM) is a prevalent gynecological condition whose etiology remains incompletely understood. This study aimed to investigate the potential mechanisms of LINC01315 in EM. This study recruited 150 EM patients and 150 healthy controls, with RT-qPCR used to detect the relative expression of target molecules. Cell proliferation, migration, and invasion were assessed using CCK-8 and Transwell assays, respectively. Inflammatory cytokines were quantified via ELISA. The targeted interaction between miR-497-5p and LINC01315/BDNF was validated through RIP and dual luciferase assays. Functional networks downstream of miR-497-5p were analyzed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway databases. LINC01315 exhibited significantly elevated expression in EM, correlating with progressively higher visual analogue scale (VAS) scores of dysmenorrhea and revised American Society for Reproductive Medicine (rASRM) staging, demonstrating strong diagnostic efficacy. LINC01315 knockdown markedly suppressed the proliferation, migration, and invasion of hEM15A cells. It also reduced the expression and secretion of key inflammatory factors, including IL-6, TNF-α, and IL-1β. Mechanistically, LINC01315 targeted miR-497-5p. In EM patients, miR-497-5p was downregulated while BDNF expression was elevated. Furthermore, miR-497-5p specifically suppressed BDNF expression. Functional experiments confirmed that miR-497-5p inhibitors reversed the inhibitory effects of LINC01315 knockdown on the malignant phenotype and inflammatory cytokine secretion in hEM15A cells, while re-knocking down BDNF reinstated the inhibitory effects. LINC01315 promoted EM progression by adsorbing miR-497-5p and relieving its inhibition on BDNF .