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. 2023 Jun 15;22:96. doi: 10.1186/s12943-023-01801-2

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© The Author(s) 2023

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/. The Creative Commons Public Domain Dedication waiver (http://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.

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Fig. 3 — The mechanisms by which cancer stem cells generate radioresistance. This diagram shows how CSCs can self-renew upon differentiation, become quiescent, be involved in tumorigenesis, and generate immunosuppressive signals as well as exert possible effects of DNA damage repair, low ROS levels, apoptosis, autophagy, and epithelial–mesenchymal transitions in tumor stem cell–associated radioresistance. In addition, several active signaling pathways (e.g., Wnt Notch Hedgehog TGF-ß PI3K/AKT/mTOR) may also be closely related to tumor stem cell radioresistance. EMT: epithelial–mesenchymal transition, ROS: reactive oxygen species, TGF-β: transforming growth factor-β, PD-L1: programmed cell death ligand 1, IL-10: interleukin 10, Bcl-2: B-cell lymphoma-2