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Cellular Mechanism of Newly Synthesized Indoledione Derivative-induced Immunological Death of Tumor Cell
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  • Cellular Mechanism of Newly Synthesized Indoledione Derivative-induced Immunological Death of Tumor Cell
  • Cellular Mechanism of Newly Synthesized Indoledione Derivative-induced Immunological Death of Tumor Cell
저자명
Oh. Su-Jin,Ryu. Chung-Kyu,Baek. So-Young,Lee. Hyun-Ah
간행물명
Immune network : official journal of the Korean association of immunobiologists
권/호정보
2011년|11권 6호|pp.383-389 (7 pages)
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

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 $100{mu}M$) 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.