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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. 3 — TGF-β1 derived from stromal fibroblasts promotes BLCA cell migration, invasion, and EMT. A, B A wound healing assay shows that CAF-CM and NF-CM significantly enhance the migration ability of T24 cells; TGF-β1 neutralizing antibody attenuates this pro-migration effect. C, D A transwell assay suggests that CAF-CM and NF-CM markedly improve the invasive ability of T24 cells; TGF-β1 neutralizing antibody effectively reduced this pro-invasion effect. qRT-PCR (E) and WB (F, G) show that CAF-CM and NF-CM induce EMT in BLCA cells by downregulating the expression of E-cadherin and upregulating the expression of N-cadherin and Vimentin. E–G The TGF-β1 neutralizing antibody significantly attenuated these pro-EMT effects