LINC01140/miR-200c-3p and LINC01550/miR-363-3p networks play pivotal role in orchestrating progression of endometriosis

Endometriosis has been increasingly associated with the aberrant regulation of non-coding RNAs (ncRNAs), particularly long non-coding RNAs (lncRNAs) and microRNAs (miRNAs). Despite the growing recognition of their biological significance, the precise molecular mechanisms and functional roles of lncRNAs LINC01140 and LINC01550 in the pathogenesis of endometriosis remain largely unexplored. In this study, we performed an integrative bioinformatics analysis utilizing the Gene Expression Omnibus dataset to systematically identify differentially expressed lncRNAs, miRNAs, and messenger RNAs (mRNAs), thereby constructing a comprehensive competing endogenous RNA (ceRNA) regulatory network. Primary endometrial stromal cells were meticulously isolated from ectopic and ovarian endometriotic lesions, and the RNA expression profiles were rigorously validated through RT-PCR. The subcellular localization of lncRNAs was precisely determined using fluorescence in situ hybridization, while the molecular interactions between lncRNAs and miRNAs were elucidated through dual-luciferase reporter assays. To delineate the functional impact, we conducted a series of assays including Western blot analysis to evaluate cellular proliferation, migration, and apoptotic processes. Our findings reveal that the LINC01140/miR-200c-3p and LINC01550/miR-363-3p regulatory networks are markedly upregulated in the cytoplasmic compartment of endometriotic cells, exerting pivotal roles in the progression of the disease. Importantly, the targeted silencing of lncRNAs or the overexpression of miR-363-3p/miR-200c-3p significantly attenuated cellular proliferation and migration, while concurrently inducing apoptosis. These results provide compelling evidence for the critical regulatory mechanisms orchestrated by lncRNAs in endometriosis, thereby establishing a robust theoretical framework for the development of innovative therapeutic interventions targeting ncRNA-mediated pathways.