Cytoplasmic Retention of the p53 Tumor Suppressor Gene Product Is Observed in the Hepatitis B Virus X Gene-Transfected Cells

Oncogene. 1997 Oct 16;15(16):1895-901. doi: 10.1038/sj.onc.1201369.

Abstract

It has been suggested that hepatitis B virus (HBV) X gene activates X gene expression by disrupting the function of p53 tumor suppressor gene (Takada et al., 1996). To find out their connection, effect of X protein expression on the nuclear localization of p53 protein in human hepatoma cells was examined by the immunofluorescent double-staining technique. The location of transiently-expressed p53 protein was examined in X gene-transfected cells, where X protein was detected in the cytoplasm. The nuclear location of transiently-expressed p53 protein was changed to the cytoplasm by X protein co-expression. Endogenous p53 protein was also observed in the cytoplasm by X protein expression. The transcriptional activation domain of X protein and the carboxy-terminal region of p53 protein were found mutually responsible for the cytoplasmic retention of p53 protein in X gene-transfected cells. Therefore, the cytoplasmic retention of p53 protein may be closely correlated to the function of X protein expressed in transfected cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biological Transport
  • Cell Nucleus / metabolism
  • Cytoplasm / metabolism*
  • Humans
  • Trans-Activators / genetics*
  • Trans-Activators / metabolism
  • Transfection
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Trans-Activators
  • Tumor Suppressor Protein p53
  • hepatitis B virus X protein