Please use this identifier to cite or link to this item: http://nopr.niscair.res.in/handle/123456789/25163
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dc.contributor.authorKwon, Haw-Young-
dc.contributor.authorKim, Kyoung-Sook-
dc.contributor.authorAn, Hyun-Kyu-
dc.contributor.authorMoon, Hyung-In-
dc.contributor.authorKim, Hyun-Jun-
dc.contributor.authorLee, Young-Choon-
dc.date.accessioned2013-12-27T11:26:05Z-
dc.date.available2013-12-27T11:26:05Z-
dc.date.issued2013-12-
dc.identifier.issn0975-0959 (Online); 0301-1208 (Print)-
dc.identifier.urihttp://hdl.handle.net/123456789/25163-
dc.description485-491en_US
dc.description.abstractTriptolide, a diterpene derived from Tripterygium wilfordii Hook f., a Chinese medicinal herb, has been reported to inhibit cell proliferation and induce apoptosis in various human cancer cells, but its anticancer effects on human osteosarcoma cells have not yet been elucidated. In this study, we investigated whether triptolide induces apoptosis in human osteosarcoma cells and the underlying molecular mechanisms. We firstly demonstrated that triptolide inhibited cell growth and induced apoptosis in U2OS cells. Western blot analysis showed that the levels of procaspase-8, -9, Bcl-2, Bid and mitochondrial cytochrome c were downregulated in triptolide-treated U2OS cells, whereas the levels of Fas, FasL, Bax, cytosolic cytochrome c, cleaved caspase-3 and cleaved PARP were upregulated. These results suggest that triptolide induces apoptosis in U2OS cells by activating both death receptor and mitochondrial apoptotic pathways.en_US
dc.language.isoen_USen_US
dc.publisherNISCAIR-CSIR, Indiaen_US
dc.rights CC Attribution-Noncommercial-No Derivative Works 2.5 Indiaen_US
dc.sourceIJBB Vol.50(6) [December 2013]en_US
dc.subjectTriptolideen_US
dc.subjectU2OS cellen_US
dc.subjectApoptosisen_US
dc.titleTriptolide induces apoptosis through extrinsic and intrinsic pathways in human osteosarcoma U2OS cellsen_US
dc.typeArticleen_US
Appears in Collections:IJBB Vol.50(6) [December 2013]

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