Pyroptosis: mechanisms and diseases

Author(s): Pian Yu ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , Xu Zhang ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , Nian Liu ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , Ling Tang ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , Cong Peng ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ ^, , Xiang Chen ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ ^,

Publication date (Electronic): 29 March 2021

Journal: Signal Transduction and Targeted Therapy

Publisher: Nature Publishing Group UK

Keywords: Cancer therapy, Tumour immunology

Read this article at

ScienceOpen Publisher PMC

Bookmark

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Currently, pyroptosis has received more and more attention because of its association with innate immunity and disease. The research scope of pyroptosis has expanded with the discovery of the gasdermin family. A great deal of evidence shows that pyroptosis can affect the development of tumors. The relationship between pyroptosis and tumors is diverse in different tissues and genetic backgrounds. In this review, we provide basic knowledge of pyroptosis, explain the relationship between pyroptosis and tumors, and focus on the significance of pyroptosis in tumor treatment. In addition, we further summarize the possibility of pyroptosis as a potential tumor treatment strategy and describe the side effects of radiotherapy and chemotherapy caused by pyroptosis. In brief, pyroptosis is a double-edged sword for tumors. The rational use of this dual effect will help us further explore the formation and development of tumors, and provide ideas for patients to develop new drugs based on pyroptosis.

Related collections

Most cited references 447

Record: found
Abstract: found
Article: found

Hallmarks of Cancer: The Next Generation

Douglas Hanahan, Robert A. Weinberg (2011)

The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.

0 comments Cited 11777 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The blockade of immune checkpoints in cancer immunotherapy.

Drew M Pardoll (2012)

Among the most promising approaches to activating therapeutic antitumour immunity is the blockade of immune checkpoints. Immune checkpoints refer to a plethora of inhibitory pathways hardwired into the immune system that are crucial for maintaining self-tolerance and modulating the duration and amplitude of physiological immune responses in peripheral tissues in order to minimize collateral tissue damage. It is now clear that tumours co-opt certain immune-checkpoint pathways as a major mechanism of immune resistance, particularly against T cells that are specific for tumour antigens. Because many of the immune checkpoints are initiated by ligand-receptor interactions, they can be readily blocked by antibodies or modulated by recombinant forms of ligands or receptors. Cytotoxic T-lymphocyte-associated antigen 4 (CTLA4) antibodies were the first of this class of immunotherapeutics to achieve US Food and Drug Administration (FDA) approval. Preliminary clinical findings with blockers of additional immune-checkpoint proteins, such as programmed cell death protein 1 (PD1), indicate broad and diverse opportunities to enhance antitumour immunity with the potential to produce durable clinical responses.

0 comments Cited 5248 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Ferroptosis: an iron-dependent form of nonapoptotic cell death.

Scott J. Dixon, Kathryn Lemberg, Michael Lamprecht … (2012)

Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferroptosis is dependent upon intracellular iron, but not other metals, and is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. We identify the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes. Indeed, erastin, like glutamate, inhibits cystine uptake by the cystine/glutamate antiporter (system x(c)(-)), creating a void in the antioxidant defenses of the cell and ultimately leading to iron-dependent, oxidative death. Thus, activation of ferroptosis results in the nonapoptotic destruction of certain cancer cells, whereas inhibition of this process may protect organisms from neurodegeneration. Copyright © 2012 Elsevier Inc. All rights reserved.

0 comments Cited 4796 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Cong Peng: pengcongxy@csu.edu.cn

Xiang Chen:

ORCID: http://orcid.org/0000-0001-8187-636X

chenxiangck@126.com

Journal

Journal ID (nlm-ta): Signal Transduct Target Ther

Journal ID (iso-abbrev): Signal Transduct Target Ther

Title: Signal Transduction and Targeted Therapy

Publisher: Nature Publishing Group UK (London )

ISSN (Print): 2095-9907

ISSN (Electronic): 2059-3635

Publication date (Electronic): 29 March 2021

Publication date PMC-release: 29 March 2021

Publication date Collection: 2021

Volume: 6

Electronic Location Identifier: 128

Affiliations

[1 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, The Department of Dermatology, Xiangya Hospital, , Central South University, ; Changsha, Hunan China

[2 ]GRID grid.452223.0, ISNI 0000 0004 1757 7615, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, ; Changsha, Hunan China

[3 ]GRID grid.452223.0, ISNI 0000 0004 1757 7615, Hunan Key Laboratory of Skin Cancer and Psoriasis, Xiangya Hospital, ; Changsha, Hunan China

[4 ]GRID grid.452223.0, ISNI 0000 0004 1757 7615, Hunan Engineering Research Center of Skin Health and Disease, Xiangya Hospital, ; Changsha, Hunan China

[5 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, Xiangya Clinical Research Center for Cancer Immunotherapy, , Central South University, ; Changsha, Hunan China

Author information

Xiang Chen http://orcid.org/0000-0001-8187-636X

Article

Publisher ID: 507

DOI: 10.1038/s41392-021-00507-5

PMC ID: 8005494

PubMed ID: 33776057

SO-VID: d21a9787-15a7-4f90-9c67-cd9b8a986b0f

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 23 August 2020

Date revision received : 14 January 2021

Date accepted : 20 January 2021

Funding

Funded by: FundRef https://doi.org/10.13039/501100001809, National Natural Science Foundation of China (National Science Foundation of China);

Award ID: 81773341

Award Recipient : Cong Peng

Funded by: National Natural Science Foundation of China (National Science Foundation of China) - 81773341 [Peng] National Natural Science Foundation of China (National Science Foundation of China) - 81572679 [Peng]

Funded by: National Natural Science Foundation of China (National Science Foundation of China) - 81830096 [Chen] National Science Foundation of China | International Cooperation and Exchange Programme - 81620108024 [Chen]