Histone deacetylase inhibitor Trichostatin A enhanced the efficiency of adenovirus mediated gene transfer into non-small cell lung cancer cells

  • Park, Mi-Sun (KFDA) ;
  • Kang, Ho-Il (National Institute of Toxicological Research. Genetic Toxicology Divisio) ;
  • Lim, Sin-Ae (National Institute of Toxicological Research. Genetic Toxicology Divisio) ;
  • Jee, Seung-Wan (National Institute of Toxicological Research. Genetic Toxicology Divisio) ;
  • Eom, Mi-Ok (National Institute of Toxicological Research. Genetic Toxicology Divisio) ;
  • Ryeom, Tai-Kyung (National Institute of Toxicological Research. Genetic Toxicology Divisio) ;
  • Kim, Ok-Hee (National Institute of Toxicological Research. Genetic Toxicology Division)
  • Published : 2003.10.01

Abstract

One of the major limitations in using adenoviral vector for gene therapy is inefficient infection of host cells. The presence of coxsackievirus and adenovirus receptor (CAR) and ${\alpha}$-integrin on cell surfaces is required for efficient adenovirus infection. In this study, we investigated the effect of trichostatin A, a histone deacetylase inhibitor, on transfection efficiency after transduction of adenovirus mediated p16$\^$INK4a/ gene transfer. In our previous study, p16$\^$INK4a/ tumor suppressor gene transfer in the non-small cell lung cancer cells (A549 cells) by transduction of recombinant adenovirus (Ad5CMV-p16) resulted in significant inhibition of cancer cell proliferation. (omitted)

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