Competing Endogenous Ribonucleic Acid Networks in Cervical Cancer: Mechanisms and Clinical Implications

Cervical cancer (CC) remains a leading cause of cancer-related mortality among women, with persistent infection with high-risk human papillomavirus (HR-HPV) representing its primary etiological factor. Long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and pseudogenes can function as competing endogenous RNAs (ceRNAs) by competing with messenger RNAs (mRNAs) for binding to microRNAs (miRNAs), thereby reducing miRNA-mediated repression of target mRNAs. This review categorizes the ceRNA axes reported in CC as oncogenic or tumor-suppressive and examines their convergence on major signaling pathways, including Wnt/β-catenin, phosphoinositide 3-kinase (PI3K)/Akt, mitogen-activated protein kinase (MAPK), Hippo, and Notch, together with the strength of the supporting evidence. The roles of these networks in prognosis, resistance to cisplatin and radiotherapy, and responses to bioactive compounds are also evaluated. Most reported axes are supported primarily by cell-line experiments, whereas absolute RNA quantification is frequently unavailable and patient-level validation remains limited. Accordingly, ceRNA networks represent potential biomarkers and therapeutic targets, although additional mechanistic and clinical evidence is required to establish their clinical applicability.