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Role of the cGAS-STING pathway in radiotherapy for non-small cell lung cancer

One of the most important therapeutic interventions for non-small cell lung cancer is radiotherapy. Ionizing radiation (IR) is classified by traditional radiobiology principles as a direct cytocidal therapeutic agent against cancer, although there is growing recognition of other antitumor immunologi...

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Autores principales: Yang, Chunsheng, Liang, Yan, Liu, Ning, Sun, Meili
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10478265/
https://www.ncbi.nlm.nih.gov/pubmed/37667279
http://dx.doi.org/10.1186/s13014-023-02335-z
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author Yang, Chunsheng
Liang, Yan
Liu, Ning
Sun, Meili
author_facet Yang, Chunsheng
Liang, Yan
Liu, Ning
Sun, Meili
author_sort Yang, Chunsheng
collection PubMed
description One of the most important therapeutic interventions for non-small cell lung cancer is radiotherapy. Ionizing radiation (IR) is classified by traditional radiobiology principles as a direct cytocidal therapeutic agent against cancer, although there is growing recognition of other antitumor immunological responses induced by this modality. The most effective therapeutic combinations to harness radiation-generated antitumor immunity and enhance treatment results for malignancies resistant to existing radiotherapy regimens could be determined by a more sophisticated understanding of the immunological pathways created by radiation. Innate immune signaling is triggered by the activation of cGAS-STING, and this promotes adaptive immune responses to help fight cancer. This identifies a molecular mechanism radiation can use to trigger antitumor immune responses by bridging the DNA-damaging ability of IR with the activation of CD8 + cytotoxic T cell-mediated killing of tumors. We also discuss radiotherapy-related parameters that affect cGAS-STING signaling, negative consequences of cGAS-STING activation, and intriguing treatment options being tested in conjunction with IR to support immune activation by activating STING-signaling. Improved therapeutic outcomes will result from a better understanding of how IR promotes cGAS-STING signaling in immune-based treatment regimens that maximize radiotherapy’s anticancer effectiveness.
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spelling pubmed-104782652023-09-06 Role of the cGAS-STING pathway in radiotherapy for non-small cell lung cancer Yang, Chunsheng Liang, Yan Liu, Ning Sun, Meili Radiat Oncol Review One of the most important therapeutic interventions for non-small cell lung cancer is radiotherapy. Ionizing radiation (IR) is classified by traditional radiobiology principles as a direct cytocidal therapeutic agent against cancer, although there is growing recognition of other antitumor immunological responses induced by this modality. The most effective therapeutic combinations to harness radiation-generated antitumor immunity and enhance treatment results for malignancies resistant to existing radiotherapy regimens could be determined by a more sophisticated understanding of the immunological pathways created by radiation. Innate immune signaling is triggered by the activation of cGAS-STING, and this promotes adaptive immune responses to help fight cancer. This identifies a molecular mechanism radiation can use to trigger antitumor immune responses by bridging the DNA-damaging ability of IR with the activation of CD8 + cytotoxic T cell-mediated killing of tumors. We also discuss radiotherapy-related parameters that affect cGAS-STING signaling, negative consequences of cGAS-STING activation, and intriguing treatment options being tested in conjunction with IR to support immune activation by activating STING-signaling. Improved therapeutic outcomes will result from a better understanding of how IR promotes cGAS-STING signaling in immune-based treatment regimens that maximize radiotherapy’s anticancer effectiveness. BioMed Central 2023-09-04 /pmc/articles/PMC10478265/ /pubmed/37667279 http://dx.doi.org/10.1186/s13014-023-02335-z Text en © The Author(s) 2023 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Yang, Chunsheng
Liang, Yan
Liu, Ning
Sun, Meili
Role of the cGAS-STING pathway in radiotherapy for non-small cell lung cancer
title Role of the cGAS-STING pathway in radiotherapy for non-small cell lung cancer
title_full Role of the cGAS-STING pathway in radiotherapy for non-small cell lung cancer
title_fullStr Role of the cGAS-STING pathway in radiotherapy for non-small cell lung cancer
title_full_unstemmed Role of the cGAS-STING pathway in radiotherapy for non-small cell lung cancer
title_short Role of the cGAS-STING pathway in radiotherapy for non-small cell lung cancer
title_sort role of the cgas-sting pathway in radiotherapy for non-small cell lung cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10478265/
https://www.ncbi.nlm.nih.gov/pubmed/37667279
http://dx.doi.org/10.1186/s13014-023-02335-z
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