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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. 6 — A and B AT56 inhibited the expression of MYH9 and the activation of Wnt–β-catenin–STAT3 signaling in vitro and in vivo. C Confocal immunofluorescent images indicated the colocalization of MYH9 and GSK3-β protein in LY1 and LY3 cells. Bar = 40 μm. D CoIP assay showed the bindings between MYH9 protein and GSK3-β protein in LY1 and LY3 cells. E and F PTGDS and MYH9 inhibition decreased the ubiquitination of GSK3-β and prolonged its half-life in DLBCL. G The role of PTGDS and MYH9 inhibition on the expression of STAT3 mRNA in LY1 and LY3 cells. H ChIP assay showed the binding of TCF4 and STAT3 promoter in LY1 and LY3 cells. Data are shown as the mean ± SD. *p < 0.05; **p < 0.01; ***p < 0.001.