Published online Apr 16, 2023. doi: 10.12998/wjcc.v11.i11.2386
Peer-review started: December 26, 2022
First decision: February 8, 2023
Revised: February 23, 2023
Accepted: March 14, 2023
Article in press: March 14, 2023
Published online: April 16, 2023
Processing time: 100 Days and 23.2 Hours
Programmed cell death (PCD) is mediated by specific genes that encode signals. It can balance cell survival and death. Pyroptosis is a type of inflammatory, caspase-dependent PCD mediated by gasdermin proteins, which function in pore formation, cell expansion, and plasma membrane rupture, followed by the release of intracellular contents. Pyroptosis is mediated by caspase-1/3/4/5/11 and is primarily divided into the classical pathway, which is dependent on caspase-1, and the non-classical pathway, which is dependent on caspase-4/5/11. Inflammasomes play a vital role in these processes. The various components of the pyroptosis pathway are related to the occurrence, invasion, and metastasis of tumors. Research on pyroptosis has revealed new options for tumor treatment. This article summarizes the recent research progress on the molecular mechanism of pyroptosis, the relationship between the various components of the pyroptosis pathway and cancer, and the applications and prospects of pyroptosis in anticancer therapy.
Core Tip: Pyroptosis is a type of inflammatory caspase-dependent programmed cell death mediated by gasdermin proteins, which function in pore formation, cell swelling, and cell membrane rupture. This review discusses the classical and non-classical pathways of pyroptosis and the recent research progress on the molecular mechanisms of pyroptosis. We also review the relationship between various pyroptosis pathway components and different cancers, including nucleotide-binding oligomerization domain-like receptor thermal protein domain associated protein 3 inflammasomes, interleukin (IL)-18, IL-1β, and absent in melanoma 2. The potential applications of this form of cell death as a cancer treatment approach are also explored.