Cervical cancer (CC) ranks among the primary causes of cancer fatalities in women, with cisplatin (DDP) resistance significantly impacting clinical outcomes. NADH dehydrogenase (ubiquinone) FA8 (NDUFA8) is significantly upregulated in CC tissues and correlates with lower survival rates, but its role in cisplatin sensitivity in CC is still unclear. NDUFA8 silencing inhibited CC cell viability, promoted ferroptosis, evidenced by increased Fe and lipid ROS levels, along with decreased levels of ATP and reduced activities of complex I, aconitase (ACO), and xanthine oxidase (XO). However, overexpression of NDUFA8 promoted CC cell viability, inhibited ferroptosis, and increased levels of ATP and activities of complex I, ACO, and XO in ferric ammonium citrate (FAC) or rotenone-treated CC cells. NDUFA8 expression showed a negative correlation with the DDP therapy response in CC tissues and cell lines. However, in CC tissues, NDUFA8 expression was positively associated with ACO and XO activities. In in vivo experiments, the overexpression of NDUFA8 diminished the anti-tumor effects of DDP, which was counteracted by FAC. NDUFA8 promotes cell viability and inhibits ferroptosis and DDP sensitivity by stabilizing Fe-S clusters in CC.