p53-mediated cellular response to DNA damage in cells with replicative hepatitis B virus

Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1342-6. doi: 10.1073/pnas.92.5.1342.

Abstract

Wild-type p53 acts as a tumor suppressor gene by protecting cells from deleterious effects of genotoxic agents through the induction of a G1/S arrest or apoptosis as a response to DNA damage. Transforming proteins of several oncogenic DNA viruses inactivate tumor suppressor activity of p53 by blocking this cellular response. To test whether hepatitis B virus displays a similar effect, we studied the p53-mediated cellular response to DNA damage in 2215 hepatoma cells with replicative hepatitis B virus. We demonstrate that hepatitis B virus replication does not interfere with known cellular functions of p53 protein.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Base Sequence
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins / genetics
  • DNA Damage*
  • DNA Primers / chemistry
  • Doxorubicin / pharmacology
  • Gene Expression Regulation, Neoplastic / drug effects
  • Gene Expression Regulation, Viral
  • Hepatitis B / genetics*
  • Hepatitis B virus / genetics
  • Humans
  • Molecular Sequence Data
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / pharmacology*
  • Virus Replication

Substances

  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • DNA Primers
  • Tumor Suppressor Protein p53
  • Doxorubicin