This study investigates the role of STEAP3 in ovarian cancer (OC) progression through the regulation of ferroptosis via the p53/SLC7A11 pathway. STEAP3, a gene related to iron transport and redox regulation, was found to be highly expressed in OC tissues and associated with poor patient prognosis. Knockdown of STEAP3 significantly reduced the proliferation and migration of OC cells, inducing ferroptosis. Mechanistically, STEAP3 knockdown activated the p53 pathway, leading to increased ferroptosis markers such as ROS levels, decreased SOD and GPX activities, and increased MDA content. Further experiments showed that p53 activation was essential for STEAP3-induced ferroptosis, as knockdown of p53 reversed the effects of STEAP3 knockdown on OC cell growth and ferroptosis. In vivo experiments confirmed that STEAP3 knockdown inhibited tumor growth in nude mice by promoting ferroptosis through the p53 pathway. These findings suggest that STEAP3 is a potential therapeutic target for OC, as it regulates ferroptosis through the p53/SLC7A11 pathway, offering a novel approach for OC treatment. The study provides new insights into the molecular mechanisms underlying OC progression and highlights the potential of ferroptosis as a therapeutic strategy for OC.This study investigates the role of STEAP3 in ovarian cancer (OC) progression through the regulation of ferroptosis via the p53/SLC7A11 pathway. STEAP3, a gene related to iron transport and redox regulation, was found to be highly expressed in OC tissues and associated with poor patient prognosis. Knockdown of STEAP3 significantly reduced the proliferation and migration of OC cells, inducing ferroptosis. Mechanistically, STEAP3 knockdown activated the p53 pathway, leading to increased ferroptosis markers such as ROS levels, decreased SOD and GPX activities, and increased MDA content. Further experiments showed that p53 activation was essential for STEAP3-induced ferroptosis, as knockdown of p53 reversed the effects of STEAP3 knockdown on OC cell growth and ferroptosis. In vivo experiments confirmed that STEAP3 knockdown inhibited tumor growth in nude mice by promoting ferroptosis through the p53 pathway. These findings suggest that STEAP3 is a potential therapeutic target for OC, as it regulates ferroptosis through the p53/SLC7A11 pathway, offering a novel approach for OC treatment. The study provides new insights into the molecular mechanisms underlying OC progression and highlights the potential of ferroptosis as a therapeutic strategy for OC.