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Antiglioma effects of combined use of a baculovirual vector expressing wild‐type p53 and sodium butyrate
Author(s) -
Guo Haiyan,
Choudhury Yukti,
Yang Jing,
Chen Can,
Tay Felix Chang,
Lim Tit Meng,
Wang Shu
Publication year - 2011
Publication title -
the journal of gene medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.689
H-Index - 91
eISSN - 1521-2254
pISSN - 1099-498X
DOI - 10.1002/jgm.1522
Subject(s) - sodium butyrate , histone deacetylase , histone deacetylase inhibitor , cancer research , glioma , apoptosis , hdac11 , chemistry , butyrate , mutant , combination therapy , acetylation , pharmacology , histone , biology , biochemistry , gene , fermentation
Abstract Background Combination therapy is usually desirable for successful cancer treatment, especially in cancers that are resistant to single forms of therapy. Methods To achieve an optimal therapeutic effect against glioblastoma, we tested a strategy that combines baculovirus‐mediated transfer of the p53 tumor suppressor gene with the use of sodium butyrate, a histone deacetylase inhibitor. This strategy was designed based on the findings that the transduction efficiency of baculovirus in mammalian cells can be markedly enhanced by the addition of histone deacetylase inhibitors and that these inhibitors are effective in inducing cell cycle arrest, differentiation, or apoptosis in tumor cells. Results We observed a synergistic effect of the combination of the two treatments in provoking apoptosis in glioblastoma cells with mutant p53. In a mouse glioma xenograft model, the tumor inhibitory effect of baculovirus‐expressed p53 was significantly enhanced by co‐administration of sodium butyrate. Conclusions These findings suggest a new approach to treat glioblastoma using baculovirus‐mediated gene transfer in combination with administration of histone deacetylase inhibitor. Copyright © 2010 John Wiley & Sons, Ltd.