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. 2017 Jul 14;7:5387. doi: 10.1038/s41598-017-03299-3

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© The Author(s) 2017

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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Schematic representation of mechanisms underlying crosstalk between Wnt/β-catenin signaling and insulin signaling via Irs1 during hepatocarcinogenesis. Wnt/β-catenin signaling is activated during hepatocarcinogenesis due to somatic mutations of various genes related to Wnt/β-catenin signaling. Activated Wnt/β-catenin signaling upregulates Irs1 gene and protein expression. Upregulated Irs1, but not Irs2, enhances insulin signaling including Akt pathway and promotes the progression of HCC.