To investigate the role of Gasdermin E (GSDME) and its interaction with the PD1/PD-L1 pathway in the progression of cervical cancer, focusing on apoptosis, migration, and invasion of cancer cells. Primary and metastatic cervical cancer tissues were collected, and histological changes were observed using HE staining. Immunohistochemistry was performed to detect the expression of GSDME. The expression levels of GSDME and Caspase-3 were assessed by RT-qPCR and Western blot. GSDME was knocked down in HeLa cells, and PD1/PD-L1 inhibitors were administered. Caspase-3 expression, cell apoptosis, migration, and invasion abilities were evaluated. Subsequently, HeLa cells were co-cultured with CD8⁺ T cells, and the effects of GSDME knockdown combined with PD1/PD-L1 inhibitor treatment on Caspase-3 expression and related cellular behaviors were further assessed. Compared to primary cervical cancer tissues, the expression of GSDME and Caspase-3 was significantly lower in metastatic cervical cancer tissues. GSDME knockdown significantly inhibited the expression of Caspase-3 in HeLa cells, reduced cell apoptosis, and enhanced cell migration and invasion abilities. PD1/PD-L1 inhibitor treatment significantly upregulated the expression of GSDME and Caspase-3, promoted cell apoptosis, and inhibited cell migration and invasion, reversing the inhibition of apoptosis caused by GSDME knockdown. After co-culturing with CD8⁺ T cells and PD1/PD-L1 inhibitor treatment, GSDME expression and cell apoptosis significantly increased, while migration and invasion significantly decreased. Levels of perforin, granzyme B, and IFN-γ were significantly elevated. GSDME knockdown weakened the therapeutic effects of CD8⁺ T cells and PD1/PD-L1 inhibitors. GSDME plays a pivotal role in regulating apoptosis, migration, and invasion in cervical cancer, particularly in the context of the PD1/PD-L1 pathway. Targeting GSDME and PD1/PD-L1 interactions may offer a novel therapeutic strategy for metastatic cervical cancer.