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. 2021 Dec 20;13(1):16. doi: 10.1038/s41419-021-04461-6

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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. 7 — Scheme diagram depicting the underlying mechanism involved in metastasis of CRC mediated by CAFs. CAFs-derived IL-6 is able to activate JAK2-STAT3 in cancer cells. As a master transcriptional factor, STAT3 directly binds to LRG1 promoter, thus leading to upregulation of LRG1. LRG1 further promotes migration, invasion as well as EMT which is crucial for CAFs-mediated metastasis of CRC.