Effects of a histone deacetylase inhibitor, sodium butyrate, on 53-kDa protein expression and sensitivity to anticancer drugs of pancreatic cancer cells.

Abstract

Several tumor-suppressor genes, such as 53-kDa protein (p53), are inactivated in some pancreatic cancers. The lack of a functional p53 has been proposed to be a component of resistance to chemotherapy, resulting in the inhibition of apoptosis. Therefore, reintroduction of wild-type p53 is a commonly used gene therapy strategy for the treatment of various types of cancer, including pancreatic cancer.