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. 2017 Dec 22;37(10):1354–1368. doi: 10.1038/s41388-017-0026-x

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, and provide a link to the Creative Commons license. You do not have permission under this license to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 5 — RNAseq identifies transcriptional changes enriched in PI3K signaling following loss of KMT2D. a A Venn diagram depicting the overlapping DEGs in PC-3 cells transduced with two siRNAs against KMT2D vs. siControl-treated PC-3 cells (top) and heatmaps showing the top 10% of overlapping DEGs (bottom). b, c Pathway enrichment identified by KEGG b and GSEA c analysis of the DEGs between KMT2D-depleted PC-3 and siControl cells. d Western blot analysis of Akt and phospho-Akt (S473 and T308), p-BRCA1, p-CREB, and p-GSK3β after KMT2D knockdown in PC-3 and DU145 cells. e GSEA analysis of the DEGs enriched in prostate carcinogenesis, Akt upregulated, and breast cancer metastasis downregulated pathway