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. 2017 Mar 13;6(3):e300. doi: 10.1038/oncsis.2017.3

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Copyright © 2017 The Author(s)

Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Overexpression of FAM83A activates multiple CSC-associated signaling pathways. (a) Gene set enrichment analysis (GSEA) plot showing the positive correlations between high FAM83A expression and TGF-β/Smad and Wnt/β-catenin pathway gene signatures (KARAKAS_TGFB1_SIGNALING; KARLSSON_TGFB_TARGETS_UP; TRACTOME_SIGNALING_BY WNT; LABBE_TARGETSOF TGFB1_AND_WNT3A_UP) in published TCGA data sets (n=178). (b) Relative luciferase activity of TGF-β reporter and TOP/FOP reporter genes. (c) Western blotting (WB) analysis of p-Smad3 (Ser423/425) and nuclear β-catenin in the indicated cells; α-tubulin was used as the loading control. (d) WB of p-Smad3 and nuclear β-catenin expression in ten freshly isolated pancreatic cancer tissues; α-tubulin was used as the loading control. (e) Histograms (right) of the mean number of spheres formed by FAM83A-transduced cells treated with a TGF-β inhibitor and/or β-catenin inhibitor. Each bar represents the mean±s.d. of three independent experiments; *P<0.05.