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. 2021 Feb 19;12(2):200. doi: 10.1038/s41419-021-03488-z

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© The Author(s) 2021

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. 1 — a Kyoto encyclopedia of genes and genomes (KEGG) analysis of statistically significant deregulated genes in HCCs harboring c-MYC amplification, showing a significant gene clustering of TGFβ signaling pathway (P = 0.027). b Higher mRNA expression of TGFβ downstream target genes (E2F5, RHOA, RBX1 and PPP2R1A) in c-MYC amplified (MYC Amp; n = 64) HCCs than that in c-MYC non-amplified (MYC Wt; n = 293) HCCs. Student t test was applied for statistical analysis, **P < 0.01, ***P < 0.001, ****P < 0.0001. c Western blotting results showing upregulation of p-Smad2/3 in c-Myc murine HCCs (c-Myc Tumor) compared with non-tumorous normal livers (NL). β-Actin and Gapdh were used as loading controls. d Microarray analysis of mRNA expressions of TGFβ downstream target genes (E2f5, Rhoa, Rbx1, and Ppp2r1a) in c-Myc murine HCCs (c-Myc tumor and non-tumorous normal liver, NL). Student t test was applied for statistical analysis. *P < 0.05, **P < 0.01, ***P < 0.001.