Please use this identifier to cite or link to this item: https://doi.org/10.1016/S0090-8258(03)00396-2
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dc.titleResistance to Fas-mediated cell death in BeWo and NJG choriocarcinoma cell lines: Implications in immune privilege
dc.contributor.authorRajashekhar, G.
dc.contributor.authorLoganath, A.
dc.contributor.authorRoy, A.C.
dc.contributor.authorMongelli, J.M.
dc.date.accessioned2013-04-10T02:59:13Z
dc.date.available2013-04-10T02:59:13Z
dc.date.issued2003
dc.identifier.citationRajashekhar, G., Loganath, A., Roy, A.C., Mongelli, J.M. (2003). Resistance to Fas-mediated cell death in BeWo and NJG choriocarcinoma cell lines: Implications in immune privilege. Gynecologic Oncology 91 (1) : 89-100. ScholarBank@NUS Repository. https://doi.org/10.1016/S0090-8258(03)00396-2
dc.identifier.issn00908258
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/36942
dc.description.abstractObjective. An immune privileged site occurs when the allogenic tissue grafts have the propensity for prolonged survival in the host tissue. In this context, the survival and proliferation of malignant trophoblasts in the gravid uterus are currently unclear. In a previous study, we documented that Fas and FasL are coexpressed in choriocarcinoma [Gynecol. Oncol. (2003)]. This study was conducted to examine the role of the Fas/FasL pathway in immune privilege of BeWo and NJG choriocarcinoma cells in culture. Methods. The ability of anti-Fas mAb (CH-11) to sensitize choriocarcinoma cell lines to Fas-mediated cytotoxicity was assessed by MTT assays. Coculture experiments with Fas-sensitive Jurkat cells were used to demonstrate functional FasL from choriocarcinoma. RT-PCR was used to assess the expression of cFLIP. Results. The mean cell viability of BeWo and NJG cells declined to about 58 and 63% compared to controls after 72 h of culture in the presence of anti-Fas mAb (CH-11) while the Fas-sensitive Jurkat cells showed viability of only 10%. This resistance to Fas-mediated apoptosis in choriocarcinoma cells is reversed in the presence of cycloheximide (0.5 μg/ml) which further decreased the viability to 36 and 32%, respectively, at a dose of 300 ng/ml (P < 0.05). The observed resistance to Fas-mediated apoptosis therefore could be attributed to the short-lived endogenous inhibitor, cFLIP as demonstrated by the RT-PCR technique. In coculture experiments, FasL from choriocarcinoma cells induced apoptosis in the Fas-sensitive Jurkat cells, thereby indicating the capacity to evade immune attack. Conclusion. Decreased sensitivity to Fas-mediated apoptosis and counterattacking the lymphocytes may impart immune privilege in these malignant trophoblasts for prolonged survival in the host. © 2003 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/S0090-8258(03)00396-2
dc.sourceScopus
dc.subjectApoptosis
dc.subjectcFLIP
dc.subjectCycloheximide
dc.subjectFasL
dc.subjectImmune privilege
dc.typeArticle
dc.contributor.departmentOBSTETRICS & GYNAECOLOGY
dc.description.doi10.1016/S0090-8258(03)00396-2
dc.description.sourcetitleGynecologic Oncology
dc.description.volume91
dc.description.issue1
dc.description.page89-100
dc.description.codenGYNOA
dc.identifier.isiut000185731200013
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