LINC00702 promotes the proliferative, migratory and invasive phenotypes of endometrial stromal cells in endometriosis via the miR-103a-3p/FGF2 ceRNA axis

Abstract Background To investigate the expression pattern of LINC00702 in endometriosis and explore its regulatory role and molecular mechanism in endometrial stromal cells (ESCs). Methods Eutopic and ectopic tissues from 84 endometriosis patients and normal tissues from 72 controls were collected. Primary normal endometrial stromal cells (NESCs) and ectopic endometrial stromal cells (EcESCs) were isolated and cultured. LINC00702, miR-103a-3p, and FGF2 expression were detected by RT-qPCR. Cell proliferation, apoptosis, migration, and invasion were assessed by CCK-8, flow cytometry, and Transwell assays. Subcellular localization, dual-luciferase reporter assays, and rescue experiments were performed to validate the LINC00702/miR-103a-3p/FGF2 regulatory axis. Results LINC00702 was upregulated in ectopic endometrial tissues and EcESCs. Overexpression of LINC00702 enhanced the proliferative, anti‑apoptotic, migratory, and invasive phenotypes of NESCs, while silencing LINC00702 reversed these phenotypes in EcESCs. miR-103a-3p was downregulated in endometriosis and could reverse the regulatory effect of LINC00702 on ESCs. FGF2 was a direct target of miR-103a-3p, which was highly expressed in endometriosis and positively correlated with LINC00702. FGF2 knockdown reversed the effect of LINC00702 overexpression on NESCs, while FGF2 overexpression rescued the inhibitory effect of LINC00702 silencing on EcESCs. Conclusion LINC00702 promotes proliferative, anti‑apoptotic, migratory, and invasive phenotypes of ESCs in endometriosis through the LINC00702/miR-103a-3p/FGF2 ceRNA regulatory axis, providing potential therapeutic targets for endometriosis treatment.