Background Cervical cancer remains a major global health burden among women. Persistent infection with high-risk human papillomavirus (HR-HPV) is the primary driver of cervical carcinogenesis, yet additional cellular regulatory processes are required for tumor progression. Ferroptosis, an iron-dependent form of regulated cell death, has been implicated in cancer metabolism and therapeutic response. However, the involvement of ferroptosis-related long non-coding RNAs (FRLs) in human papillomaviru