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Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy
In recent years, immunotherapy represented by immune checkpoint inhibitors (ICIs) has led to unprecedented breakthroughs in cancer treatment. However, the fact that many tumors respond poorly or even not to ICIs, partly caused by the absence of tumor-infiltrating lymphocytes (TILs), significantly li...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9208265/ https://www.ncbi.nlm.nih.gov/pubmed/35725836 http://dx.doi.org/10.1038/s41392-022-01046-3 |
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author | Gao, Weitong Wang, Xueying Zhou, Yang Wang, Xueqian Yu, Yan |
author_facet | Gao, Weitong Wang, Xueying Zhou, Yang Wang, Xueqian Yu, Yan |
author_sort | Gao, Weitong |
collection | PubMed |
description | In recent years, immunotherapy represented by immune checkpoint inhibitors (ICIs) has led to unprecedented breakthroughs in cancer treatment. However, the fact that many tumors respond poorly or even not to ICIs, partly caused by the absence of tumor-infiltrating lymphocytes (TILs), significantly limits the application of ICIs. Converting these immune “cold” tumors into “hot” tumors that may respond to ICIs is an unsolved question in cancer immunotherapy. Since it is a general characteristic of cancers to resist apoptosis, induction of non-apoptotic regulated cell death (RCD) is emerging as a new cancer treatment strategy. Recently, several studies have revealed the interaction between non-apoptotic RCD and antitumor immunity. Specifically, autophagy, ferroptosis, pyroptosis, and necroptosis exhibit synergistic antitumor immune responses while possibly exerting inhibitory effects on antitumor immune responses. Thus, targeted therapies (inducers or inhibitors) against autophagy, ferroptosis, pyroptosis, and necroptosis in combination with immunotherapy may exert potent antitumor activity, even in tumors resistant to ICIs. This review summarizes the multilevel relationship between antitumor immunity and non-apoptotic RCD, including autophagy, ferroptosis, pyroptosis, and necroptosis, and the potential targeting application of non-apoptotic RCD to improve the efficacy of immunotherapy in malignancy. |
format | Online Article Text |
id | pubmed-9208265 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-92082652022-06-21 Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy Gao, Weitong Wang, Xueying Zhou, Yang Wang, Xueqian Yu, Yan Signal Transduct Target Ther Review Article In recent years, immunotherapy represented by immune checkpoint inhibitors (ICIs) has led to unprecedented breakthroughs in cancer treatment. However, the fact that many tumors respond poorly or even not to ICIs, partly caused by the absence of tumor-infiltrating lymphocytes (TILs), significantly limits the application of ICIs. Converting these immune “cold” tumors into “hot” tumors that may respond to ICIs is an unsolved question in cancer immunotherapy. Since it is a general characteristic of cancers to resist apoptosis, induction of non-apoptotic regulated cell death (RCD) is emerging as a new cancer treatment strategy. Recently, several studies have revealed the interaction between non-apoptotic RCD and antitumor immunity. Specifically, autophagy, ferroptosis, pyroptosis, and necroptosis exhibit synergistic antitumor immune responses while possibly exerting inhibitory effects on antitumor immune responses. Thus, targeted therapies (inducers or inhibitors) against autophagy, ferroptosis, pyroptosis, and necroptosis in combination with immunotherapy may exert potent antitumor activity, even in tumors resistant to ICIs. This review summarizes the multilevel relationship between antitumor immunity and non-apoptotic RCD, including autophagy, ferroptosis, pyroptosis, and necroptosis, and the potential targeting application of non-apoptotic RCD to improve the efficacy of immunotherapy in malignancy. Nature Publishing Group UK 2022-06-20 /pmc/articles/PMC9208265/ /pubmed/35725836 http://dx.doi.org/10.1038/s41392-022-01046-3 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Review Article Gao, Weitong Wang, Xueying Zhou, Yang Wang, Xueqian Yu, Yan Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy |
title | Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy |
title_full | Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy |
title_fullStr | Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy |
title_full_unstemmed | Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy |
title_short | Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy |
title_sort | autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9208265/ https://www.ncbi.nlm.nih.gov/pubmed/35725836 http://dx.doi.org/10.1038/s41392-022-01046-3 |
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