Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/86465
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dc.contributor.authorHuang, Mao-Hsuanzh_TW
dc.contributor.authorLin, Shinn-Zongzh_TW
dc.contributor.authorLin, Po-Chengzh_TW
dc.contributor.authorChiou, Tzyy-Wenzh_TW
dc.contributor.authorHarn, Yeu-Weizh_TW
dc.contributor.authorHo, Li-Ingzh_TW
dc.contributor.authorChan, Tzu-Minzh_TW
dc.contributor.authorChou, Chih-Weizh_TW
dc.contributor.authorChuang, Chang-Hanzh_TW
dc.contributor.authorSu, Hong-Linzh_TW
dc.contributor.authorHarn, Horng-Jyhzh_TW
dc.date2014-
dc.date.accessioned2015-08-04T05:57:32Z-
dc.date.available2015-08-04T05:57:32Z-
dc.identifier.issn1010-4283zh_TW
dc.identifier.issn1423-0380zh_TW
dc.identifier.issn1423-0380zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/86465-
dc.description.abstractDeveloping an effective drug for treating human glioblastoma multiform (GBM) has been investigated persistently. A pure compound butylidenephthalide (BP), isolated from Angelica sinensis, has been shown the activities to arrest the growth and initiate apoptosis of GBM in our previous reports. In this study, we further demonstrated that BP treatment accelerates the cell senescence in a dose-dependent manner in vitro and in vivo. S-phase kinase-associated protein 2 (Skp2), a proto-oncogene, is generally upregulated in cancer. We found that it was downregulated in BP-treated GBM cells. The downregulation of Skp2 is parallel with increasing p16 and p21 expression which causes G0/G1 arrest and tumor cell senescence. We also found that restoring the Skp2 protein level by exogenous overexpression prevents the BP-induced cell senescence. Therefore, the linkage between cell senescence and Skp2 expression is strengthened. Promoter binding analysis further detailed that the BP-mediated SP1 reduction might involve in the Skp2 downregulation. In summary, these results emphasize that BP-triggered senescence in GBM cells is highly associated with its control on Skp2 regulation.zh_TW
dc.language.isoenzh_TW
dc.relationTumor Biology, Volume 35, Issue 5, Page(s) 4875-4884.zh_TW
dc.subjectAnimalszh_TW
dc.subjectBrain Neoplasmszh_TW
dc.subjectCell Agingzh_TW
dc.subjectCell Line, Tumorzh_TW
dc.subjectCell Proliferationzh_TW
dc.subjectCell Survivalzh_TW
dc.subjectDown-Regulationzh_TW
dc.subjectGlioblastomazh_TW
dc.subjectHumanszh_TW
dc.subjectMicezh_TW
dc.subjectMice, Nudezh_TW
dc.subjectPhthalic Anhydrideszh_TW
dc.subjectS-Phase Kinase-Associated Proteinszh_TW
dc.subjectSp1 Transcription Factorzh_TW
dc.titleBrain tumor senescence might be mediated by downregulation of S-phase kinase-associated protein 2 via butylidenephthalide leading to decreased cell viabilityzh_TW
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1007/s13277-014-1639-0zh_TW
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.fulltextno fulltext-
item.languageiso639-1en-
item.grantfulltextnone-
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