Cellular Mechanism of Newly Synthesized Indoledione Derivative-induced Immunological Death of Tumor Cell
Immune Network
; : 383-389, 2011.
Article
em En
| WPRIM
| ID: wpr-60135
Biblioteca responsável:
WPRO
ABSTRACT
BACKGROUND: EY-6 is one of the newly synthesized indoledione derivatives to induce tumor cell-specific cell death. In this study, we investigated the mechanism of immunological death induced by EY-6 at mouse colon cancer cell as well as at the normal immune cell represented by dendritic cell. METHODS: C57BL/6 mouse syngeneic colon cancer cell MC38 was treated with EY-6, and analyzed by MTT for viability test, flow cytometry for confirming surface expressing molecules and ELISA for detection of cytokine secretion. Normal myeloid-dendritic cell (DC) was ex vivo cultured from bone marrow hematopoietic stem cells of C57BL/6 mice with GM-CSF and IL-4 to analyze the DC uptake of dead tumor cells and to observe the effect of EY-6 on the normal DC. RESULTS: EY-6 killed the MC38 tumor cells in a dose dependent manner (25, 50 and 100 microM) with carleticulin induction. And EY-6 induced the secretion of IFN-gamma but not of TNF-alpha from the MC38 tumor cells. EY-6 did not kill the ex-vivo cultured DCs at the dose killing tumor cells and did slightly but not significantly induced the DC maturation. The OVA-specific cross-presentation ability of DC was not induced by chemical treatment (both MHC II and MHC I-restricted antigen presentation). CONCLUSION: Data indicate that the EY-6 induced tumor cell specific and immunological cell death by modulation of tumor cell phenotype and cytokine secretion favoring induction of specific immunity eliminating tumor cells.
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Base de dados:
WPRIM
Assunto principal:
Fenótipo
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Medula Óssea
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Células Dendríticas
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Ensaio de Imunoadsorção Enzimática
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Células-Tronco Hematopoéticas
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Fator Estimulador de Colônias de Granulócitos e Macrófagos
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Interleucina-4
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Fator de Necrose Tumoral alfa
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Morte Celular
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Neoplasias do Colo
Limite:
Animals
Idioma:
En
Revista:
Immune Network
Ano de publicação:
2011
Tipo de documento:
Article