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. 2016 Jan 12;5(1):7. doi: 10.3390/jcm5010007

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© 2016 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).

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Phosphorylated Smad2/3 signaling fibro-carcinogenesis. As human hepatitis virus-related chronic liver diseases progress, chronic inflammation and hepatitis virus additively shift hepatocytic Smad phospho-isoform signaling from tumor-suppressive pSmad3C to the fibro-carcinogenic pSmad3L and pSmad2L/C pathway. Anti-viral therapy can reverse phospho-Smad signaling from fibro-carcinogenesis to tumor suppression. Type 2 EMT promotes liver fibrosis induced by chronic inflammation. Type 3 EMT exacerbates the HCC phenotype by upregulating invasive and metastatic potential.