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. 2025 Mar 18;23:347. doi: 10.1186/s12967-025-06322-8

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© The Author(s) 2025

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 2 — Wnt5a promotes bicalutamide resistance of prostate cancer cells. (A, B) Comparison of the sensitivity of bicalutamide-resistant LNCaP cell line (LNCaP-BicR) and LNCaP parental cell line (LNCaP-Parental) to bicalutamide by MTS assay. (C) Protein and mRNA levels of Wnt5a in LNCaP-BicR cells and LNCaP-Parental cells were detected by Western blot analysis and RT-qPCR. (D) The inhibitory effect of bicalutamide on LNCaP cells with or without Wnt5a overexpression was tested by colony formation assay and (E, F) MTS assay. (G, H) The inhibitory effect of bicalutamide on 22RV1 cells with or without Wnt5a knockdown was tested by MTS assay. *P < 0.05; **P < 0.01