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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. 2 — The diversity of CAF subtypes is regulated by complex molecular mechanisms, including genetic regulation mediated by tumor cell-derived factors, epigenetic modulation via direct contact between tumor cells and CAFs, and metabolic reprogramming reflecting the reverse Warburg effect. Moreover, these mechanisms can work independently or cooperatively to shape the stromal structure and function, resulting in tumor restraining or tumor supportive effects of CAF subsets in a context-dependent manner. SOCS1: Suppressor of cytokine signaling; STAT3: Signal transducer and activator of transcription 3; LDH: Lactate dehydrogenase; PYCR1: pyrroline-5-carboxylate reductase 1.