Cervical squamous cell carcinoma (CESC) is the fourth most common malignancy and the fourth leading cause of cancer deaths in women worldwide. Despite advances in treatment, cisplatin-based radiotherapy remains the primary treatment option. However, cisplatin resistance is a major challenge, leading to poor prognosis. Therefore, understanding the molecular mechanisms underlying cisplatin resistance is crucial for developing novel therapeutic strategies. Through bioinformatics analysis, we investigated the expression of CDKN2A in the CESC database. WB, IHC, qPCR, and CCK-8 were used for clinical analysis of CDKN2A expression and its correlation with CESC cell proliferation. Through qPCR, CCK-8, ROS, MDA, Fe and WB, we explored how CDKN2A promotes cisplatin resistance by inhibiting ferroptosis. In nude mouse tumor experiments, we investigated how CDKN2A participates in ferroptosis and cisplatin resistance in CESC through the JAK2/STAT3 pathway. Furthermore, we explored CDKN2A as a target of METTL3 and how YTHDF1 enhances the stability of m6A-modified CDKN2A. We investigated the role of CDKN2A in CESC and its involvement in cisplatin resistance. We found that CDKN2A expression was associated with CESC cell ferroptosis and cisplatin resistance. Mechanistically, CDKN2A was identified as a target of METTL3, and YTHDF1 enhanced the stability of m6A-modified CDKN2A. Furthermore, METTL3 inhibited ferroptosis through m6A modification of YTHDF1/CDKN2A, influencing cisplatin resistance in CESC. Our findings provide new insights into the molecular mechanisms of cisplatin resistance in CESC and suggest that targeting the METTL3/YTHDF1/CDKN2A axis may be a promising strategy to overcome this resistance and improve treatment outcomes.