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

M. C. Jiang, S. F. Luo, L. T. Li, C. C. Lin, S. Y. Du, C. Y. Lin, Y. W. Hsu, Ching Fong Liao*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

18 Scopus citations

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-γ/adriamycin treatment in Hep G2 cells. Our data showed that Hep G2 cells treated with combined interferon-γ/adriamycin enhanced cell apoptosis in comparison with that of cells treated with adriamycin. Interferon-γ 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-γ did not increase p53 accumulation; nevertheless it enhanced adriamycin-induced p53 accumulation. Overexpression of IRF-1 augmented the combined interferon-γ/adriamycin-induced p53 accumulation. Interferon-γ co-treatment increased the stability of p53 protein induced by adriamycin. Our data suggest that TNF-γ may greatly enhance the combined interferon-γ/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-γ-based chemo-immunotherapy of the chemotherapy- resistant cancers.

Original languageEnglish
Pages (from-to)91-99
Number of pages9
JournalJournal of Experimental and Clinical Cancer Research
Volume26
Issue number1
StatePublished - 03 2007

Keywords

  • Adriamycin
  • Apoptosis
  • CAS
  • Interferon-γ
  • P53
  • TNFR-1

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