Journal
MOLECULAR CELL
Volume 81, Issue 22, Pages 4579-4590Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2021.09.003
Keywords
-
Categories
Funding
- Ministry of Science and Technology of Taiwan [MOST 109-2327-B-039-003, MOST 110-2639-B-039-001-ASP, MOST 109-2314-B-039-006-MY2]
- China Medical University YingTsai Young Scholar Award [CMU108-YTY-02]
- Higher Education Sprout Project - Cancer Prevention & Research Institutes of Texas [RP160710-P2]
- Cancer Center support grant [NCI NIH P30 CA016672]
- National Institutes of Health [5R01 AI116722]
- Breast Cancer Research Foundation [BCRF 20-070]
- Higher Education Sprout Project - Ministry of Education of Taiwan [RP160710-P2]
Ask authors/readers for more resources
ICP and CCP are processes of cell pyroptosis activated by different molecular mechanisms, affecting antitumor immunity and therapeutic outcomes.
Canonically, gasdermin D (GSDMD) cleavage by caspase-1 through inflammasome signaling triggers immune cell pyroptosis (ICP) as a host defense against pathogen infection. However, cancer cell pyroptosis (CCP) was recently discovered to be activated by distinct molecular mechanisms in which GSDMB, GSDMC, and GSDME, rather than GSDMD, are the executioners. Moreover, instead of inflammatory caspases, apoptotic caspases and granzymes are required for gasdermin protein cleavage to induce CCP. Sufficient accumulation of protease-cleaved gasdermin proteins is the prerequisite for CCP. Inflammation induced by ICP or CCP results in diametrically opposite effects on antitumor immunity because of the differential duration and released cellular contents, leading to contrary effects on therapeutic outcomes. Here, we focus on the distinct mechanisms of ICP and CCP and discuss the roles of ICP and CCP in inflammation and antitumor immunity, representing actionable targets.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available
Share Paper
