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. 2015 Feb 3;2(4):e1001199. doi: 10.1080/23723556.2014.1001199

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 1. — Boosting NAD⁺ as a strategy to prevent and cure hepatocellular carcinoma. Increased expression of unconventional prefoldin RPB5 interactor (URI) in response to inflammatory cues inhibits aryl hydrocarbon receptor (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in de novo nicotinamide adenine dinucleotide (NAD⁺) synthesis, thereby causing DNA damage at early stages of tumorigenesis and hepatocellular carcinoma (HCC) development. Boosting NAD⁺ pools prevents DNA damage and tumor formation and cures early HCC.