Cervical cancer (CC) is one of the severe cancers that pose a threat to women’s health and result in death. CENPF, the centromere protein F, plays a crucial role in mitosis by regulating numerous cellular processes, such as chromosome segregation during mitosis. According to bioinformatics research, CENPF serves as a master regulator that is upregulated and activated in cervical cancer. Nevertheless, the precise biological mechanism that CENPF operates in CC remains unclear. The aim of this study was to analyze the function of CENPF on cervical cancer and its mechanism. We conducted immunohistochemistry and western blot analysis to examine the expression levels of CENPF in both cervical cancer tissues and cells. To explore the hidden biological function of CENPF in cell lines derived from CC, we applied lentivirus transfection to reduce CENPF manifestation. CENPF’s main role is to regulate ferroptosis which was assessed by analyzing Reactive Oxygen Species (ROS), malonaldehyde (MDA), etc. The vitro findings were further validated through a subcutaneous tumorigenic nude mouse model. Our research finding indicates that there is an apparent upregulation of CENPF in not merely tumor tissues but also cell lines in the carcinomas of the cervix. In vitro and vivo experimental investigations have demonstrated that the suppression of CENPF can impede cellular multiplication, migration, and invasion while inducing ferroptosis. The ferroptosis induced by CENPF inhibition in cervical cancer cell lines is likely mediated through the Nrf2/HO-1 pathway. The data herein come up with the opinion that CENPF may have a crucial role in influencing anti-cervical cancer effects by inducing ferroptosis via the triggering of the Nrf2/HO-1 signaling pathway.

宫颈癌（CC）是威胁妇女健康并导致死亡的严重癌症之一。 CENPF（着丝粒蛋白 F）通过调节许多细胞过程（例如有丝分裂期间的染色体分离）在有丝分裂中发挥着至关重要的作用。根据生物信息学研究，CENPF 作为主调节因子，在宫颈癌中上调和激活。然而，CENPF 在 CC 中发挥作用的精确生物学机制仍不清楚。本研究旨在分析CENPF对宫颈癌的作用及其机制。我们进行了免疫组织化学和蛋白质印迹分析来检查宫颈癌组织和细胞中 CENPF 的表达水平。为了探索 CENPF 在 CC 来源的细胞系中隐藏的生物学功能，我们应用慢病毒转染来减少 CENPF 的表现。 CENPF的主要作用是调节铁死亡，通过分析活性氧（ROS）、丙二醛（MDA）等来评估其作用。通过皮下致瘤裸鼠模型进一步验证了体外研究结果。我们的研究结果表明，CENPF 不仅在肿瘤组织中明显上调，而且在宫颈癌的细胞系中也有明显的上调。体外和体内实验研究表明，抑制 CENPF 可以阻碍细胞增殖、迁移和侵袭，同时诱导铁死亡。宫颈癌细胞系中 CENPF 抑制诱导的铁死亡可能是通过 Nrf2/HO-1 途径介导的。本文的数据得出的观点是，CENPF 可能通过触发 Nrf2/HO-1 信号通路诱导铁死亡，在影响抗宫颈癌作用方面发挥关键作用。