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. 2023 Jul 3;55(7):1322–1332. doi: 10.1038/s12276-023-01013-0

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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 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/.

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Fig. 3 — Current strategies to selectively target tumor-promoting CAFs include (a) blocking the differentiation from precursor cells to tumor-promoting CAFs via inhibition of precursor activation or targeting key signaling pathways in differentiation. b Targeted depletion of tumor-promoting CAFs without affecting tumor-restraining CAFs through genetic manipulation or specific antibodies. c Induction of phenotypic switching from tumor-promoting to tumor-restraining CAFs. d Targeting the crosstalk between cancer cells and tumor-promoting CAFs to inhibit their supportive effect on cancer proliferation, migration and chemoresistance.