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
; 26(1): 91-9, 2007 Mar.
Article
em En
| MEDLINE
| ID: mdl-17550137
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.
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Base de dados:
MEDLINE
Assunto principal:
Doxorrubicina
/
Proteína Supressora de Tumor p53
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Interferon gama
/
Apoptose
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Carcinoma Hepatocelular
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Proteína de Suscetibilidade a Apoptose Celular
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Receptores Tipo I de Fatores de Necrose Tumoral
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Neoplasias Hepáticas
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Antineoplásicos
Limite:
Humans
Idioma:
En
Ano de publicação:
2007
Tipo de documento:
Article