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. 2014 Sep 11;13:210. doi: 10.1186/1476-4598-13-210

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© Holla et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Model. TNF-α regulates the progression of cancers by promoting p53-dependent apoptosis. However, the presence of BCG induces SHH signaling-dependent expression of COP1, a regulator of p53 activity. COP1 targets p53 for ubiquitin-mediated proteasomal degradation. These events culminate into inhibition of apoptosis and promotion of tumorigenicity.