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. 2023 Jul 17;21:475. doi: 10.1186/s12967-023-04303-3

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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 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. 8 — TGF-β1/FAP/VCAN axis promotes stromal fibroblast-mediated EMT in bladder cancer in vivo. A–C Subcutaneous xenograft models were established by co-injecting T24 cells with fibroblasts, which demonstrated that stromal fibroblasts facilitate tumor formation and growth in vivo. CAF has a stronger tumor-promoting effect than NF. Overexpression of FAP enhanced the tumor-promoting effects of stromal fibroblasts, while knockdown of FAP weakened those effects. Immunohistochemistry (D), immunofluorescence (E, G), and WB (F) showed that TGF-β1/FAP/VCAN axis regulates bladder cancer EMT in vivo. CAF has a stronger EMT-inducing effect than NF. Overexpression of FAP enhanced the EMT-inducing effects of stromal fibroblasts, while knockdown of FAP weakened those effects