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. 2023 Jan 4;30:1. doi: 10.1186/s12929-022-00894-z

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© The Author(s) 2023

Open AccessThis 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. 1 — CAFs regulate tumor progression and therapeutic response. Our recent work demonstrated that CAFs promote tumor progression and therapeutic resistance through diverse mechanisms. CAFs secrete IL6 and IL8, which activate the JAK2-STAT3 pathway. JAK2-dependent phosphorylated BRD4 interacts with STAT3 to modulate chromatin remodeling (enhancer/super-enhancer reprogramming) and promote oncogene expression, leading to BETi resistance and tumor progression. IL6 also induces LRG1 expression through STAT3-dependent transactivation, which promotes EMT and metastasis. CAF-secreted TGF-β2 induced the expression of GLI2, which synergizes with hypoxia-induced HIF1α to promote CRC stemness and chemoresistance