Exploring the Role of MED12 in Ferroptosis of Gastric Signet-Ring Cell Carcinoma

Background Gastric signet-ring cell carcinoma (GSRCC) is a highly invasive subtype of gastric cancer characterized by poor prognosis and resistance to treatment. Given the important role of ferroptosis in cancer progression, this study aims to explore the function of the transcriptional regulatory factor MED12 in the regulation of ferroptosis in GSRCC and its effects on cell proliferation and metastasis. Methods We employed siRNA-mediated knockdown and overexpression experiments in KATOⅢ cells to assess the impact of MED12 on cellular proliferation and invasion, as well as ferroptosis indicators such as GPX4, GSH, Fe²⁺, and ROS levels. Additionally, we utilized CCK8 assays for cell viability, Transwell assays for invasion potential, and flow cytometry for ROS detection. Results Our findings demonstrate that MED12 overexpression significantly enhances the proliferation and invasion of KATOⅢ cells, while MED12 knockdown substantially diminishes these capacities. Correspondingly, knockdown of MED12 resulted in decreased levels of GPX4 and GSH levels, along with heightened Fe²⁺ and ROS levels, indicating its inhibitory role on ferroptosis. The application of Ferrostatin-1, a ferroptosis inhibitor, further corroborated that MED12 regulates cellular responses through this ferroptotic pathway. Conclusions These results reveal the key role of MED12 in ferroptosis by regulating iron metabolism and oxidative stress, providing new biomarkers and targets for the treatment of GSRCC. Future research should further validate the clinical application potential of MED12 and explore its related signaling pathways, aiming to improve treatment outcomes for GSRCC patients.