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. 2021 Nov 6;29(3):642–656. doi: 10.1038/s41418-021-00880-2

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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 — A Wnt3a impaired the cytotoxicity of AT56 in LY1 and LY3 cells. B and C Wnt3a rescued the cell cycle arrest and cell apoptosis promotion caused by AT56. D The inhibition of the Wnt–β-catenin-STAT3 pathway by AT56 was reversed with Wnt3a. E WP1066 reversed the proliferation promotion caused by PTGDS overexpression. F WP1066 enhanced the effect of AT56 on cell proliferation in LY1 cells (2.5 μM) and LY3 cells (1 μM). G WP1066 enhanced the effect of AT56 on cell apoptosis in LY1 cells and LY3 cells. H and I Blebbistatin reversed the increased proliferation and the activation of Wnt–β-catenin–STAT3 signaling caused by PTGDS overexpression without change of PTGDS expression. Data are shown as the mean ± SD. *p < 0.05; **p < 0.01; ***p < 0.001.