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. 2022 Oct 25;15:153. doi: 10.1186/s13045-022-01364-7

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© The Author(s) 2022

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. 4 — Main associations between B7-H3 and CAFs, tumor cells and other TME cells. Activated B7-H3 increases the proliferation, progression and migration of CAFs and inhibits the apoptosis of CAFs. Inhibiting B7-H3 in gastric cancer decreases the expression of IL-6, CXCL12, FGF1 and VEGF and suppresses the migration of CAFs. B7-H3 activation also promotes tumor cell growth and enhances tumor cell metastasis through AKT pathways. B7-H3 modulates cytokine secretion in many types of TME cells, including T cells, endothelial cells and CAFs, and B7-H3 helps to remodel the ECM by activating MMP2/MMP9. TME, tumor microenvironment; CAFs, cancer-associated fibroblasts; MSCs, mesenchymal stromal cells; ECM, extracellular matrix