인터루킨-18수용체 형질도입 자궁경부암 세포주에서의 Fas 매개 세포사멸에 대한 저항성 및 활성 산소종의 상향조절에 관한 연구

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dc.contributor.authorDo Young Yoon-
dc.contributor.authorJ W Park-
dc.contributor.authorJ W Kim-
dc.date.accessioned2017-04-19T09:01:00Z-
dc.date.available2017-04-19T09:01:00Z-
dc.date.issued2003-
dc.identifier.issnI000-0170-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/6463-
dc.description.abstractBackground : The fas (CD95/Apo-1)/Fas ligand (FasL) system is reported to be involved in the suppression and stimulation of immune responses, and the reactive oxygen species (ROS) play a key role in the mechanism for resisting Fas-induced apoptosis of tumor cells. In this work, we investigated the effect of endogenous interleukin (IL)-18 on the regulation of immune related factors such as Fas/ Fas ligand and intercellular adhesion molecules (ICAM), and of the ROS level in IL-18 receptor (IL18R) transfected C-33A cells. Methods : The cervical cancer cell line C-33A was transfected with IL-18R (C-33A/IL-18R). For the detection of pro-inflammatory cytokines in C-33A/IL-18R, reverse-transcriptase (RT) polymerase chain reaction (PCR), in situ enzyme-linked immunosorbent assay (ELISA), Western blot, and Northern blot analyses were performed. The level of p53 was determined by Western blot. Intracellular ROS, ICAM1, FasL, and apoptosis in C-33A/IL-18R were measured by flow cytometry. Results : In situ ELISA and RT-PCR showed that, among pro-inflammatory cytokines, IL-18 was induced in C-33A/IL-18R whereas there appeared no induction of the IL-1 , IL-1 , tumor necrosis factor (TNF)- , and IL-6. IL-18R transfection showed a slight enhancement of the Fas via upregulation of intracellular ROS and IL-18 in C-33A cells whereas there was no effect on the expression of p53, ICAM-1 and FasL. However, treatment with the agonistic anti-Fas antibody showed that the enhanced surface Fas was not functional or was not enough to induce apoptosis and the C-33A/IL18R cells escaped still resistant to Fas-mediated apoptosis. Conclusions : IL-18R transfection induced IL-18 expression and enhanced ROS and Fas expression in C-33A cells. These results show that C-33A/IL-18R cells escaped from immunuosurveillance by failure to express ICAM-1 adhesion molecules and Fas ligand, and are resistant to Fas-mediated apoptosis. (Korean J Lab Med 2003; 23: 455-63)-
dc.publisherKorea Soc-Assoc-Inst-
dc.title인터루킨-18수용체 형질도입 자궁경부암 세포주에서의 Fas 매개 세포사멸에 대한 저항성 및 활성 산소종의 상향조절에 관한 연구-
dc.title.alternativeUpregulation of reactive oxygen species and resistance to fas-mediated apoptosis in cervical cancer cell lines transfected with the IL-18 receptor-
dc.typeArticle-
dc.citation.titleKorean Journal of Laboratory Medicine-
dc.citation.number6-
dc.citation.endPage463-
dc.citation.startPage455-
dc.citation.volume23-
dc.contributor.affiliatedAuthorDo Young Yoon-
dc.contributor.alternativeName윤도영-
dc.contributor.alternativeName박주원-
dc.contributor.alternativeName김종완-
dc.identifier.bibliographicCitationKorean Journal of Laboratory Medicine, vol. 23, no. 6, pp. 455-463-
dc.subject.keywordIL-18-
dc.subject.keywordFas-
dc.subject.keywordFas/FasL-
dc.subject.keywordIL-18R-
dc.subject.localIL-18-
dc.subject.localFAS-
dc.subject.localFas-
dc.subject.localfas-
dc.subject.localFas/FasL-
dc.subject.localIL-18R-
dc.description.journalClassY-
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