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Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression

Hearing loss-associated protein gasdermin E (GSDME), an effector of secondary necrosis, has been identified in a new pathway of programmed cell death (PCD). GSDME epigenetic silencing and mutations resulting in loss-of-function have been reported in cancer tissues. Additionally, GSDME upregulation i...

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Autores principales: Wang, Yueyuan, Peng, Jingyu, Xie, Xiao, Zhang, Zhihao, Li, Mingxi, Yang, Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8317517/
https://www.ncbi.nlm.nih.gov/pubmed/34335940
http://dx.doi.org/10.7150/jca.48989
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author Wang, Yueyuan
Peng, Jingyu
Xie, Xiao
Zhang, Zhihao
Li, Mingxi
Yang, Ming
author_facet Wang, Yueyuan
Peng, Jingyu
Xie, Xiao
Zhang, Zhihao
Li, Mingxi
Yang, Ming
author_sort Wang, Yueyuan
collection PubMed
description Hearing loss-associated protein gasdermin E (GSDME), an effector of secondary necrosis, has been identified in a new pathway of programmed cell death (PCD). GSDME epigenetic silencing and mutations resulting in loss-of-function have been reported in cancer tissues. Additionally, GSDME upregulation inhibits tumor proliferation as well as colony forming ability, and reduces the incidence of lymphatic metastasis, demonstrating that GSDME may act as a tumor suppressor. Here, we have focused on the molecular mechanisms of GSDME-mediated PCD, and tried to reveal the crosstalk between this cell death pathway and apoptosis, autophagy, GSDMD-mediated pyroptosis. Moreover, we concluded the anti-cancer activity of GSDME include forming permeable membranes, and triggering anti-cancer immunity. Thus, GSDME was potential to be a novel target for cancer prevention and treatment.
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spelling pubmed-83175172021-07-29 Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression Wang, Yueyuan Peng, Jingyu Xie, Xiao Zhang, Zhihao Li, Mingxi Yang, Ming J Cancer Review Hearing loss-associated protein gasdermin E (GSDME), an effector of secondary necrosis, has been identified in a new pathway of programmed cell death (PCD). GSDME epigenetic silencing and mutations resulting in loss-of-function have been reported in cancer tissues. Additionally, GSDME upregulation inhibits tumor proliferation as well as colony forming ability, and reduces the incidence of lymphatic metastasis, demonstrating that GSDME may act as a tumor suppressor. Here, we have focused on the molecular mechanisms of GSDME-mediated PCD, and tried to reveal the crosstalk between this cell death pathway and apoptosis, autophagy, GSDMD-mediated pyroptosis. Moreover, we concluded the anti-cancer activity of GSDME include forming permeable membranes, and triggering anti-cancer immunity. Thus, GSDME was potential to be a novel target for cancer prevention and treatment. Ivyspring International Publisher 2021-06-26 /pmc/articles/PMC8317517/ /pubmed/34335940 http://dx.doi.org/10.7150/jca.48989 Text en © The author(s) https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Review
Wang, Yueyuan
Peng, Jingyu
Xie, Xiao
Zhang, Zhihao
Li, Mingxi
Yang, Ming
Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression
title Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression
title_full Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression
title_fullStr Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression
title_full_unstemmed Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression
title_short Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression
title_sort gasdermin e-mediated programmed cell death: an unpaved path to tumor suppression
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8317517/
https://www.ncbi.nlm.nih.gov/pubmed/34335940
http://dx.doi.org/10.7150/jca.48989
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