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Gasdermin E suppresses tumour growth by activating anti-tumour immunity
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Journal Article
Gasdermin E suppresses tumour growth by activating anti-tumour immunity
2020
Overview
Cleavage of the gasdermin proteins to produce pore-forming amino-terminal fragments causes inflammatory cell death (pyroptosis)
1
. Gasdermin E (GSDME, also known as DFNA5)—mutated in familial ageing-related hearing loss
2
—can be cleaved by caspase 3, thereby converting noninflammatory apoptosis to pyroptosis in GSDME-expressing cells
3
–
5
.
GSDME
expression is suppressed in many cancers, and reduced GSDME levels are associated with decreased survival as a result of breast cancer
2
,
6
, suggesting that GSDME might be a tumour suppressor. Here we show that 20 of 22 tested cancer-associated GSDME mutations reduce GSDME function. In mice, knocking out
Gsdme
in GSDME-expressing tumours enhances, whereas ectopic expression in
Gsdme
-repressed tumours inhibits, tumour growth. This tumour suppression is mediated by killer cytotoxic lymphocytes: it is abrogated in perforin-deficient mice or mice depleted of killer lymphocytes. GSDME expression enhances the phagocytosis of tumour cells by tumour-associated macrophages, as well as the number and functions of tumour-infiltrating natural-killer and CD8
+
T lymphocytes. Killer-cell granzyme B also activates caspase-independent pyroptosis in target cells by directly cleaving GSDME at the same site as caspase 3. Uncleavable or pore-defective GSDME proteins are not tumour suppressive. Thus, tumour GSDME acts as a tumour suppressor by activating pyroptosis, enhancing anti-tumour immunity.
The gasdermin E protein is shown to act as a tumour suppressor: it is cleaved by caspase 3 and granzyme B and leads to pyroptosis of cancer cells, provoking an immune response to the tumour.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/31
/ 13/95
/ 14/19
/ 38/23
/ 38/77
/ 42/41
/ 42/44
/ 64/60
/ 82/1
/ 82/29
/ 82/83
/ 96/106
/ Aging
/ Animals
/ Breast
/ Cancer
/ Female
/ Humanities and Social Sciences
/ Humans
/ Immunity
/ Melanoma
/ Mice
/ Mutation
/ Perforin
/ Proteins
/ Receptors, Estrogen - chemistry
/ Receptors, Estrogen - genetics
/ Receptors, Estrogen - metabolism
/ Science
/ T-Lymphocytes, Cytotoxic - immunology
/ Tumors
