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Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 [M. K., M. E. G., S. B., T. F.], and First Department of Surgery, Faculty of Medicine, Kagoshima University, Kagoshima 890-8520, Japan [T. A.]
The presence of coxsackie and adenovirus receptor (CAR) and
v integrin on cell surfaces is required for efficient
adenovirus infection. Treatment of cells with the histone deacetylase
inhibitor FR901228 (depsipeptide) increased CAR and
v
integrin RNA levels in six cancer cell lines. Sodium butyrate and
trichostatin A, other histone deacetylase inhibitors, caused similar
increases. Cells treated with FR901228 prior to infection had a
410-fold increase in transgene expression from a
ß-galactosidase-expressing adenoviral vector. These studies
suggest that FR901228 increases the efficiency of adenoviral transgene
expression and may be useful in cancer gene therapy.
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