Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/71523
DC FieldValueLanguage
dc.contributor.authorTu, W.C.en_US
dc.contributor.authorWu, C.C.en_US
dc.contributor.authorHsieh, H.L.en_US
dc.contributor.authorChen, C.Y.en_US
dc.contributor.authorHsu, S.L.en_US
dc.date2008zh_TW
dc.date.accessioned2014-06-11T06:01:50Z-
dc.date.available2014-06-11T06:01:50Z-
dc.identifier.issn0041-0101zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/71523-
dc.description.abstractHoneybee (Apis mellifera) venom (BV) has been reported to exhibit anticancer effects, but its mode of action at the cellular and molecular levels remains largely unknown. We found that honeybee venom induced apoptosis in human melanoma A2058 cells but not in normal skin fibroblast Detroit 551 cells. The BV-induced apoptosis was accompanied by generation of reactive oxygen species and alteration of mitochondrial membrane potential transition. Treatment with antioxidants significantly attenuated BV-induced apoptosis. Although caspase-2 and -3 were slightly activated by BV, inhibitors of caspase-2 and -3 could not block BV-induced apoptosis in A2058 cells. Data from immunostaining indicated that EncloG and AIF were translocated from mitochondria to the cytosol or nucleus, suggesting that BV induces apoptosis in A2058 cells via a caspase-independent pathway. In addition, cJun N-terminal kinases (JNK) and ERK were rapidly activated after a 5 min incubation with BV, while p38 and AKT were inactivated after 30 min administration of BV. Inhibition of JNK significantly attenuated BV-triggered apoptotic death. Moreover, BV induced a rapid and marked increase in cytosolic calcium ion. Incubation of cells under calcium-free conditions effectively diminished BV-induced apoptosis. Furthermore, when the calcium-free treatment was combined with ouabain, the recovery of cellular calcium fluctuation protected A2058 cells against BV-induced apoptosis. Finally, treatment of A2058 cells with melittin, the major component of BV, resulted in similar elevation of calcium levels and cell killing effects, suggesting that melittin is the major determinant in BV-triggered cell death. These observations provide a molecular explanation for the antiproliferative properties of BV, and suggest that this agent may be useful in treating melanoma. (C) 2008 Elsevier Ltd. All rights reserved.en_US
dc.language.isoen_USzh_TW
dc.relationToxiconen_US
dc.relation.ispartofseriesToxicon, Volume 52, Issue 2, Page(s) 318-329.en_US
dc.relation.urihttp://dx.doi.org/10.1016/j.toxicon.2008.06.007en_US
dc.subjectbee venomen_US
dc.subjectmelanomaen_US
dc.subjectcalciumen_US
dc.subjectouabainen_US
dc.subjectapoptosisen_US
dc.subjectbee venomen_US
dc.subjectrheumatoid-arthritisen_US
dc.subjectsteroid-hormoneen_US
dc.subjectin-vitroen_US
dc.subjectproliferationen_US
dc.subjectmelittinen_US
dc.subjectcanceren_US
dc.subjectgrowthen_US
dc.subjectca2+en_US
dc.subjectactivationen_US
dc.titleHoneybee venom induces calcium-dependent but caspase-independent apoptotic cell death in human melanoma A2058 cellsen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/j.toxicon.2008.06.007zh_TW
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.fulltextno fulltext-
item.languageiso639-1en_US-
item.grantfulltextnone-
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