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. 2019 Nov 14;38:467. doi: 10.1186/s13046-019-1462-y

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 5 — Silencing Wnt10b after knockout of NSD1 inhibits the formation and metastasis of tumors by inactivating the Wnt/β-catenin signaling pathway. a, Representative images of tumor formation through nude mouse xenograft model. b, Volume and weight of tumors. c, Pulmonary metastasis (× 200) detected by HE staining. d, TOPFlash luciferase activity in vivo after NSD1 knockout and silencing Wnt10b. e, Positive cell rates of β-catenin, C-myc, and CyclinD1 in tumors (× 400) detected by immunohistochemical staining. * p < 0.05 vs. the vector group (nude mice treated with vector). Data (mean ± s.d.) among multiple groups were analyzed by one-way ANOVA, followed by Tukey’s post-hoc test, while data at different time points were analyzed by repeated measures ANOVA, followed by the Bonferroni’s post-hoc test, n = 12