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SIRT1, a nicotinamide adenine dinucleotide<jats:sup>+<\/jats:sup>\u2010dependent histone\/protein deacetylase, plays a crucial role in various physiological processes, such as aging, metabolism, neurogenesis and apoptosis, owing to its ability to deacetylate numerous substrates, such as histone and NF\u2010\u03baB, which is implicated as an exacerbation factor in ATL. Here, we assessed how SIRT1 is regulated in primary ATL cells and leukemic cell lines. SIRT1 expression in ATL patients was significantly higher than that in healthy controls, especially in the acute type. Sirtinol, a SIRT1 inhibitor, induced significant growth inhibition or apoptosis in cells from ATL patients and leukemic cell lines, especially HTLV\u20101\u2010related cell lines. Sirtinol\u2010induced apoptosis was mediated by activation of the caspase family and degradation of SIRT1 in the nucleus. Furthermore, SIRT1 knockdown by SIRT1\u2010specific small interfering RNA caused apoptosis <jats:italic>via<\/jats:italic> activation of caspase\u20103 and PARP in MT\u20102 cells, HTLV\u20101\u2010related cell line. These results suggest that SIRT1 is a crucial antiapoptotic molecule in ATL cells and that SIRT1 inhibitors may be useful therapeutic agents for leukemia, especially in patients with ATL.<\/jats:p>","DOI":"10.1002\/ijc.27481","type":"journal-article","created":{"date-parts":[[2012,2,9]],"date-time":"2012-02-09T13:08:07Z","timestamp":1328792887000},"page":"2044-2055","source":"Crossref","is-referenced-by-count":74,"title":["High expression of the longevity gene product SIRT1 and apoptosis induction by sirtinol in adult T\u2010cell leukemia 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