Mechanistic insights into HAGLROS-mediated therapy resistance in ovarian cancer

Ovarian cancer is a deadly gynecological malignancy, often detected late with frequent recurrence and treatment resistance. Non-coding RNAs, particularly long non-coding RNAs (lncRNAs), are now recognized as crucial regulators of cancer pathogenesis. This review synthesizes current literature to elucidate the molecular and functional roles of the lncRNA HAGLROS in ovarian cancer, focusing on its interactions within competing endogenous RNA (ceRNA) networks. HAGLROS, located at 2q31.1, is an oncogenic lncRNA that promotes ovarian cancer progression. It drives enhanced cell proliferation, metastasis, and chemotherapy resistance while inhibiting apoptosis. Its oncogenic activity is primarily mediated through intricate sponging interactions with microRNAs (miRNAs), disrupting post-transcriptional gene regulation and influencing epigenetic and transcriptional processes. The dysregulation of HAGLROS underscores its significant role in ovarian tumorigenesis. Its ability to modulate key cancer hallmarks via miRNA interactions reveals complex regulatory axes central to the disease's pathogenesis. HAGLROS represents a promising candidate for early diagnostic biomarkers and novel therapeutic interventions. Further investigation into the HAGLROS–miRNA–mRNA network is essential for defining its clinical utility and developing targeted treatments for ovarian cancer.