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

被引：0
作者：
Jiang, M. C. [1 ]
Luo, S. F. [1 ]
Li, L. T. [1 ]
Lin, C. C. [1 ]
Du, S. Y. [1 ]
Lin, C. Y. [1 ]
Hsu, Y. W. [1 ]
Liao, C. F. [1 ]
机构：
[1] Acad Sinica, Inst Cellular & Organism Biol, Taipei 11529, Taiwan
来源：
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH | 2007年 / 26卷 / 01期
关键词：
adriamycin; apoptosis; CAS; interferon-gamma; p53; TNFR-1;
D O I：
暂无
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
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-gamma increased TNFR-1, CSE1L/CAS (cellular apoptosis susceptibility protein), Bax, and Bad levels. Adriamycin increased p53 and Bax, but not TNFR-I and CAS levels. Interferon-gamma 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-7 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, p 53, Bax, and Bad may be the targets for the interferon-gamma-based chemo-immunotherapy of the chemotherapy-resistant cancers.
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页码：91 / 99
页数：9
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