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Effect of trichostatin A on cell growth and expression of cell cycle‐ and apoptosis‐related molecules in human gastric and oral carcinoma cell lines
Author(s) -
Suzuki Tetsuo,
Yokozaki Hiroshi,
Kuniyasu Hiroki,
Hayashi Ken,
Naka Kazuhito,
Ono Shigehiro,
Ishikawa Takenori,
Tahara Eiichi,
Yasui Wataru
Publication year - 2000
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(20001215)88:6<992::aid-ijc24>3.0.co;2-9
Subject(s) - trichostatin a , cell growth , cell cycle , apoptosis , biology , cell culture , microbiology and biotechnology , cell cycle checkpoint , cyclin b1 , cyclin d1 , histone deacetylase , cancer research , chemistry , histone , cyclin dependent kinase 1 , biochemistry , genetics , gene
Abstract The effect of trichostatin A (TSA), histone deacetylase inhibitor, on cell growth and the mechanism of growth modulation was examined in 8 gastric and 3 oral carcinoma cell lines which included 9‐ cis ‐retinoic acid resistant (MKN‐7 and Ho‐1‐N‐1) and IFN‐β resistant cell lines (MKN‐7, ‐28 and ‐45). TSA inhibited growth in all cell lines examined. Apoptotic cell death was confirmed by apoptotic ladder formation and induction of a cleaved form (85 kDa) of poly (ADP‐ribose) polymerase (PARP) induction. TSA enhanced the protein expression of p21 WAF1 , CREB‐binding protein, cyclinE, cyclin A, Bak and Bax, while it reduced the expression of E2F‐1, E2F‐4, HDAC1, p53 and hyperphosphorylated form of Rb. Furthermore, TSA induced morphological changes, such as elongation of cytoplasm and cell‐to‐cell detachment, in gastric and oral carcinoma cell lines. These results suggest that TSA may inhibit cell growth and induce apoptosis of gastric and oral carcinoma cells through modulation of the expression of cell cycle regulators and apoptosis‐regulating proteins. Int. J. Cancer 88:992–997, 2000. © 2000 Wiley‐Liss, Inc.