p15INK4b in HDAC inhibitor‐induced growth arrest

FEBS Letters - Tập 554 - Trang 347-350 - 2003
Toshiaki Hitomi1, Youichirou Matsuzaki1, Tomoya Yokota1, Yuuki Takaoka1, Toshiyuki Sakai1
1Department of Molecular-Targeting Cancer Prevention, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan

Tóm tắt

Histone deacetylase (HDAC) inhibitors arrest human tumor cells at the G1 phase of the cell cycle and activate the cyclin‐dependent kinase inhibitor, p21WAF1/Cip1. However, several studies have suggested the existence of a p21WAF1/Cip1‐independent molecular pathway. We report here that HDAC inhibitors, trichostatin A (TSA) and sodium butyrate, activate the p15INK4b gene, a member of the INK4 gene family, through its promoter in HaCaT cells. Furthermore, we show that up‐regulation of p15INK4b by TSA is associated with cell growth inhibition of HCT116 p21 (−/−) cells. Our findings suggest that p15INK4b is one of the important molecular targets of HDAC inhibitors.

Tài liệu tham khảo

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FEBS Letters

Tập 554

347-350

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