Progress in the study of molecular mechanisms of cell pyroptosis in tumor therapy.

• Caspase-1-induced pyroptosis pathway of classical inflammatory vesicles. • Non-classical inflammatory vesicle scorch pathway. • Pyroptosis and digestive system malignancies. • Pyroptosis and non-small cell lung cancer. • The role and mechanism of cell scorching in antitumor therapy. Pyroptosis, also known as cellular inflammatory necrosis, is a programmed cell death mediated by the Gasdermin family of proteins. The mechanisms by which pyroptosis occurs are divided into the GSDMD-mediated Caspase-1 and Caspase-4/-5/-11-dependent classical inflammatory vesicle pathway and the GSDME-mediated Caspase-3 and granzyme-dependent non-classical inflammatory vesicle pathways, among others. Recent studies have shown that pyroptosis has both inhibitory and promotive effects on tumor development. Pyroptosis induction also plays a dual role in antitumor immunotherapy: on the one hand, it suppresses antitumor immunity by promoting the release of inflammatory factors, and on the other hand, it inhibits tumor cell proliferation by triggering antitumor inflammatory responses. In addition, cell scorching plays an essential role in chemotherapy. It has been found that natural drugs modulating the induction of cell scorch are necessary to treat tumors. Therefore, studying the specific mechanisms of cell pyroptosis in different tumors can provide more ideas for developing oncology drugs. In this paper, we review the molecular mechanisms of pyroptosis and the role of pyroptosis in tumor development and treatment to provide new targets for clinical tumor treatment, prognosis, and antitumor drug development. [ABSTRACT FROM AUTHOR]