Disulfidptosis-associated ferroptosis gene BCAT2 regulates c-MYC expression and promotes the malignant progression of epithelial ovarian cancer cells by interacting with GYS1

Purpose Epithelial ovarian cancer (EOC) is a prevalent gynecological malignancy with a notoriously poor prognosis. Recent oncological research has highlighted ferroptosis and disulfidptosis as novel forms of cell death with potential therapeutic implications. However, the relationship between these processes and their role in EOC remains poorly understood. Methods Through comprehensive bioinformatics analyses, we identified six disulfidptosis-related ferroptosis genes in EOC samples. A prognostic model was developed utilizing these genes to assess their predictive power for EOC survival prognosis. We further investigated the dual role of BCAT2 in regulating ferroptosis and modulating GYS1, which is implicated in disulfidptosis. The influence of BCAT2 on cell proliferation, migration, and invasion was examined through its regulation of c-MYC and its impact on G2M phase and EMT-related proteins. Results Our findings reveal that BCAT2 plays a pivotal role in both ferroptosis and disulfidptosis in EOC. It not only regulates ferroptosis but also modulates GYS1, thereby influencing disulfidptosis. We observed a strong correlation between BCAT2 and GYS1 expression. Additionally, BCAT2's interaction with GYS1 extends its influence beyond ferroptosis, significantly disrupting disulfidptosis as well. Conclusion This study provides valuable insights into the complex interplay between disulfidptosis and ferroptosis in EOC, our findings underscore the potential of targeting BCAT2 and GYS1 as a therapeutic strategy for EOC.