Chemotherapy drugs induce pyroptosis through caspase-3 cleavage of a gasdermin
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Summary
It is shown that GSDME, which was originally identified as DFNA5 (deafness, autosomal dominant 5), can switch caspase-3-mediated apoptosis induced by TNF or chemotherapy drugs to pyroptosis, suggesting that casp enzyme activation can trigger necrosis by cleaving G SDME and offer new insights into cancer chemotherapy.
- Type
- article
- Published
- 2017-05-01
- Cited by
- 2,798
- References
- 28
- Access
- Open access
- OpenAlex
- https://openalex.org/W2608687752
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:4397958
Keywords
Pyroptosis, Apoptosis, Programmed cell death, Caspase, Cancer research
References
- Nonsyndromic hearing impairment is associated with a mutation in DFNA5
- Inflammasomes: Mechanism of Action, Role in Disease, and Therapeutics
- Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death
- Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling
- An official American Thoracic Society workshop report: features and measurements of experimental acute lung injury in animals.
- DFNA5 (ICERE‐1) contributes to acquired etoposide resistance in melanoma cells
- Pyroptotic cell death defends against intracellular pathogens
- Identification of DFNA5 as a target of epigenetic inactivation in gastric cancer
- The expression and regulation of DFNA5 in human hepatocellular carcinoma DFNA5 in hepatocellular carcinoma
- Mutations in the gene encoding pejvakin, a newly identified protein of the afferent auditory pathway, cause DFNB59 auditory neuropathy
- Innate immune sensing of bacterial modifications of Rho GTPases by the Pyrin inflammasome
- The NLRC4 inflammasome receptors for bacterial flagellin and type III secretion apparatus
- Mice lacking Dfna5 show a diverging number of cochlear fourth row outer hair cells.
- Aberrant promoter methylation and tumor suppressive activity of the DFNA5 gene in colorectal carcinoma
- Inflammatory caspases are innate immune receptors for intracellular LPS
- The potential role of DFNA5, a hearing impairment gene, in p53-mediated cellular response to DNA damage
- A yeast model for the study of human DFNA5, a gene mutated in nonsyndromic hearing impairment.
- Methylation of the DFNA5 gene is frequently detected in colorectal cancer.
- Hypomethylating agent combination strategies in myelodysplastic syndromes: Hopes and shortcomings
- Pore-forming activity and structural autoinhibition of the gasdermin family
Cited by
- Structures of the gasdermin D C-terminal domains reveal mechanisms of autoinhibition
- Pyroptosis versus necroptosis: similarities, differences, and crosstalk
- Pattern Recognition Receptors and the Host Cell Death Molecular Machinery
- Death and fire—the concept of necroinflammation
- BIX‐01294 enhanced chemotherapy effect in gastric cancer by inducing GSDME‐mediated pyroptosis
- Caspase-3/gasdermin-E axis facilitates the progression of coronary artery calcification by inducing the release of high mobility group box protein 1.
- Chemotherapy-treated cells go up in flames
- Proteolytic control of regulated necrosis.
- Gasdermins: Effectors of pyroptosis
- The monogenic autoinflammatory diseases define new pathways in human innate immunity and inflammation
- Papers of note in Nature 547 (7661)
- Inhibition of caspase-1 or gasdermin-D enable caspase-8 activation in the Naip5/NLRC4/ASC inflammasome
- Biological events and molecular signaling following MLKL activation during necroptosis
- Molecular mechanisms of inflammasome signaling
- Inflammasomes and Cancer: The Dynamic Role of the Inflammasome in Tumor Development
- Structure insight of GSDMD reveals the basis of GSDMD autoinhibition in cell pyroptosis
- p53-dependent programmed necrosis controls germ cell homeostasis during spermatogenesis
- Emerging roles of mitochondria and autophagy in liver injury during sepsis
- The renaissance of anti‐neoplastic immunity from tumor cell demise
- Inflammatory cell death in intestinal pathologies
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