Arif, Mohammed ; Vedamurthy, Bhusainahalli M. ; Choudhari, Ramesh ; Ostwal, Yogesh B. ; Mantelingu, Kempegowda ; Kodaganur, Gopinath S. ; Kundu, Tapas K. (2010) Nitric oxide-mediated histone hyperacetylation in oral cancer: target for a water-soluble HAT inhibitor, CTK7A Chemistry & Biology, 17 (8). pp. 903-913. ISSN 1074-5521
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Official URL: http://www.cell.com/chemistry-biology/retrieve/pii...
Related URL: http://dx.doi.org/10.1016/j.chembiol.2010.06.014
Abstract
Altered histone acetylation is associated with several diseases, including cancer. We report here that, unlike in most cancers, histones are found to be highly hyperacetylated in oral squamous cell carcinoma (OSCC; oral cancer) patient samples. Mechanistically, overexpression, as well as enhanced autoacetylation, of p300 induced by nucleophosmin (NPM1) and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) causes the hyperacetylation, which is nitric oxide (NO) signal dependent. Inhibition of the histone acetyltransferase (HAT) activity of p300 by a water-soluble, small molecule inhibitor, Hydrazinocurcumin (CTK7A), substantially reduced the xenografted oral tumor growth in mice. These results, therefore, not only establish an epigenetic target for oral cancer, but also implicate a HAT inhibitor (HATi) as a potential therapeutic molecule.
| Item Type: | Article |
|---|---|
| Source: | Copyright of this article belongs to Cell Press Inc. |
| ID Code: | 18960 |
| Deposited On: | 25 Nov 2010 14:41 |
| Last Modified: | 04 Jun 2011 09:00 |
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