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. 2021 Oct 26;7:314. doi: 10.1038/s41420-021-00679-7

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© The Author(s) 2021

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. 4 — Activation of stromal Hh signalling inhibits the initiation and progression of CAC by increasing stromal anti-inflammatory cytokine IL-10 and CD4 + Foxp3+regulatory T cells. The Hh activator SAG21k can decrease colitis severity and CAC burden. Administration of the Hh antagonist, vismodegib, can facilitate CAC formation. Additionally, activated stromal Hh signalling reduces the tumour burden and tumour progression in mouse CAC models partly by reducing secreted BMP inhibitors such as Gremlin 1 (Grem1) and Noggin (Nog), and by restricting cancer stem cell (CSC) features. Arrows and blunt-ended lines indicate activation and inhibition, respectively. Hh Hedgehog, IL-10 interleukin-10, Nog Noggin, Grem1 Gremlin, BMP bone morphogenetic protein.