Synergic CSE1L/CAS, TNFR-1, and p53 apoptotic pathways in combined interferon-gamma/adriamycin-induced apoptosis of Hep G2 hepatoma cells

J Exp Clin Cancer Res. 2007 Mar;26(1):91-9.

Abstract

Many cancers are chemotherapy-resistant. Chemotherapy combined with immunotherapy offers a potential avenue for the treatment of chemotherapy-resistant cancers. In this study, we investigated the apoptotic pathways induced by combined interferon-gamma/adriamycin treatment in Hep G2 cells. Our data showed that Hep G2 cells treated with combined interferon-gamma/adriamycin enhanced cell apoptosis in comparison with that of cells treated with adriamycin. Interferon-y increased TNFR-1, CSE1L/CAS (cellular apoptosis susceptibility protein), Bax, and Bad levels. Adriamycin increased p53 and Bax, but not TNFR- 1 and CAS levels. Interferon-y did not increase p53 accumulation; nevertheless it enhanced adriamycin-induced p53 accumulation. Overexpression of IRF-1 augmented the combined interferon-gamma/adriamycin-induced p53 accumulation. Interferon-gamma co-treatment increased the stability of p53 protein induced by adriamycin. Our data suggest that TNF-gamma may greatly enhance the combined interferon-gamma/chemotherapeutic drug-induced apoptosis of cancers. Our findings also indicate that CAS, TN-FR-1, p53, Bax, and Bad may be the targets for the interferon-y-based chemo-immunotherapy of the chemotherapy-resistant cancers.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Carcinoma, Hepatocellular / metabolism*
  • Carcinoma, Hepatocellular / pathology
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cellular Apoptosis Susceptibility Protein / metabolism*
  • Dose-Response Relationship, Drug
  • Doxorubicin / pharmacology*
  • Drug Synergism
  • Etoposide / pharmacology
  • Humans
  • Interferon Regulatory Factor-1 / genetics
  • Interferon Regulatory Factor-1 / metabolism
  • Interferon-gamma / pharmacology*
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / pathology
  • Receptors, Tumor Necrosis Factor, Type I / metabolism*
  • Signal Transduction / drug effects
  • Transfection
  • Tumor Suppressor Protein p53 / metabolism*
  • bcl-2-Associated X Protein / metabolism
  • bcl-Associated Death Protein / metabolism

Substances

  • Antineoplastic Agents
  • BAD protein, human
  • BAX protein, human
  • Cellular Apoptosis Susceptibility Protein
  • Interferon Regulatory Factor-1
  • Receptors, Tumor Necrosis Factor, Type I
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • bcl-2-Associated X Protein
  • bcl-Associated Death Protein
  • Etoposide
  • Doxorubicin
  • Interferon-gamma