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p15 INK4b in HDAC inhibitor‐induced growth arrest
Author(s) -
Hitomi Toshiaki,
Matsuzaki Youichirou,
Yokota Tomoya,
Takaoka Yuuki,
Sakai Toshiyuki
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01186-4
Subject(s) - trichostatin a , hacat , sodium butyrate , cell cycle checkpoint , histone deacetylase inhibitor , histone deacetylase , chemistry , cancer research , hdac11 , histone deacetylase 5 , cell cycle , microbiology and biotechnology , histone deacetylase 2 , growth inhibition , cell growth , cell culture , gene , biology , histone , genetics , biochemistry
Histone deacetylase (HDAC) inhibitors arrest human tumor cells at the G1 phase of the cell cycle and activate the cyclin‐dependent kinase inhibitor, p21 WAF1/Cip1 . However, several studies have suggested the existence of a p21 WAF1/Cip1 ‐independent molecular pathway. We report here that HDAC inhibitors, trichostatin A (TSA) and sodium butyrate, activate the p15 INK4b gene, a member of the INK4 gene family, through its promoter in HaCaT cells. Furthermore, we show that up‐regulation of p15 INK4b by TSA is associated with cell growth inhibition of HCT116 p21 (−/−) cells. Our findings suggest that p15 INK4b is one of the important molecular targets of HDAC inhibitors.