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. 2016 Mar 28;107(5):609–618. doi: 10.1111/cas.12908

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© 2016 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Signaling pathways involving differentially expressed proteins in CD44 variant 9‐positive hepatocellular carcinomas. Note activation of nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2), with strong overexpression of its downstream proteins NAD(P)H quinone oxidoreductase (NQO1) and superoxide dismutase 2 (SOD2), as well as activation of transforming growth factor‐β (TGF ‐β) and platelet‐derived growth factor (PDGF) and inhibition of pregnane X receptor (PXR), constitutive androstane receptor (CAR), and CCAAT/enhancer binding protein (C/EBP). The illustration shows proteins with increased (red) and decreased (green) expression in CD44 variant 9‐positive hepatocellular carcinomas.