The G0/G1 switch gene 2 (G0S2) is a compact protein with diverse functions, including its involvement in apoptosis, metabolism, and inflammation. Its potential role in cancer-related apoptosis remains poorly understood.

This study aimed to investigate the underlying mechanisms of G0S2 in apoptosis, particularly in cancer.

Proteomic analysis was performed on G0S2-overexpressing mice, and functional annotations, pathway analysis, and protein-protein interactions were explored. Apoptosis was verified through TUNEL staining, immunohistochemistry, and molecular genetic strategies.

G0S2 overexpression led to significant alterations in the expression of apoptosis-related proteins, including Caspase3, FADD, and BAX. Mechanistically, G0S2 promotes apoptosis through the BAX/Caspase3 pathway.

G0S2 is implicated in apoptosis, specifically through the BAX/Caspase3 pathway, shedding light on its potential as a therapeutic target for diseases related to apoptosis, inflammation, and cancer. These findings may have implications for the development of novel therapeutic strategies for treating this devastating malignancy.