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Neuro-Oncology 2002 4(2):95-101; doi:10.1093/neuonc/4.2.95
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© 2002 by the Society forNeuro-Oncology

Histone acetylation may suppress human glioma cell proliferation whenp21WAF/Cip1 and gelsolin are induced

Hideki Kamitani1, Seijiro Taniura, Kenji Watanabe, Makoto Sakamoto, Takashi Watanabe and Thomas Eling

Department of Neurosurgery, Institute of NeurologicalSciences, Faculty of Medicine, Tottori University, Yonago, 683-8504 Japan(H.K., S.T., K.W., M.S., T.W.); Laboratory ofMolecular Carcinogenesis, National Institute of Environmental Health Sciences,Research Triangle Park, NC 27709 (S.T., T.E.)

1 Address correspondence and reprint requests to Hideki Kamitani, 36-1,Nishi-cho, Yonago, Tottori 683-8504 Japan.


  Abstract

Histone deacetylase inhibitors that increase histone acetylation ontransformed cells are being investigated as unique anticancer drugs. The aimof this investigation was to evaluate an antiproliferative activity of thehistone deacetylase inhibitors sodium butyrate (NaBT) and trichostatin A on 5glioma cell lines, T98G, A172, U-87 MG, U-118 MG, and U-373 MG, with theexamination of the altered expressions in p21 and gelsolin genes.Treatment with 5-mM NaBT and 40 ng/ml trichostatin A for 48 h caused more thana 50% growth inhibition in 5 cell lines as measured by cell proliferationassays. An increase in histone acetylation was confirmed in each cell line.After treatment with 5 mM NaBT, T98G, A172, and U118 cells undergo apoptosisas indicated by DNA ladder formation. Treatment with NaBT and trichostatin Aalso decreased DNA synthesis as examined by the fluorescence-activated cellsorting analysis in T98G and U87 cells. In addition to the suppression of cellgrowth, the up regulation of p21 and gelsolin expression was observedafter treatment with NaBT, especially in T98G cells. Maximum expression ofp21 and gelsolin was observed within 24 h after treatment. Resultsfrom our in vitro studies indicate that the treatment of human glioma cellswith one of the histone deacetylase inhibitors suppresses cell growth withdecreasing DNA synthesis and stimulates apoptosis, and that associatedmolecular mechanisms responsible for these effects include increased histoneacetylation as well as enhanced expression of p21 and gelsolin.

Received October 9, 2001; Accepted January 9, 2002


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