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. 2020 Oct 15;11(10):864. doi: 10.1038/s41419-020-03064-x

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© The Author(s) 2020

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. 5 — a The expression of Wnt/β-catenin signaling pathway key proteins in PRMT5-modified Tu686 and Tu212 cells by western blotting. b Ectopic expression of Wnt4 in Tu212 cells increased the protein levels of β-catenin in the nucleus. c Depletion of Wnt4 in Tu686 cells decreased the expression of β-catenin in the nucleus. d Western blotting showing that the ectopic expression of Wnt4 in PRMT5-silencing cells greatly restored cyclin D1, β-catenin, and MMP9 expression. e Immunofluorescence assay of the increased β-catenin nuclear translocation in PRMT5-silencing or control cells combined with Wnt4 overexpression. Scale bar, 10 µm. f–h Depletion of Wnt4 reversed PRMT5-induced cell proliferation, migration, and invasion capacities. *p < 0.05, **p < 0.01.