Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/32621
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dc.contributor.authorChen, Nian-Guen_US
dc.contributor.authorLu, Chi-Chengen_US
dc.contributor.authorLin, Yu-Hsinen_US
dc.contributor.authorShen, Wu-Chungen_US
dc.contributor.authorLai, Cheng-Hungen_US
dc.contributor.authorHo, Yung-Jenen_US
dc.contributor.authorChung, Jing-Gungen_US
dc.contributor.authorLin, Tsai-Hsiuen_US
dc.contributor.authorLin, Yung-Changen_US
dc.contributor.authorYang, Jai-Singen_US
dc.contributor.other國立中興大學獸醫系zh_TW
dc.contributor.otherNational Chung Hsing University,Department of Veterinary Medicineen_US
dc.date2011-10zh_TW
dc.date.accessioned2014-06-06T07:44:00Z-
dc.date.available2014-06-06T07:44:00Z-
dc.identifier.issn1021-335Xzh_TW
dc.identifier.urihttp://hdl.handle.net/11455/32621-
dc.description.abstractEpigallocatechin-3-gallate (EGCG), a polyphenol constituent present in green tea, has been shown to inhibit the growth of cancer cells in vitro and in vivo. However, studies regarding human bladder carcinoma cells are limited and not well investigated. Hence, our study focused on the evaluation of EGCG-triggered apoptosis in TSGH-8301 human urinary bladder carcinoma cells in vivo and in vitro as well as its related molecular mechanisms. In an in vivo study, EGCG inhibited xenograft tumor size of TSGH-8301 cells in a nude mouse model. Based on an in vitro study, EGCG resulted in morphological changes and increased growth inhibition in a dose- and time-dependent manner in TSGH-8301 cells. Furthermore, sub-G1 populations were shown and caspase-9 and -3 activities were stimulated in EGCG-treated TSGH-8301 cells. Moreover, a caspase-9 inhibitor (Z-LEHD-FMK) and a caspase-3 inhibitor (Z-DEVD-FMK) were able to reduce EGCG-stimulated caspase-9 and -3 activities, respectively. Loss of mitochondrial membrane potential (Delta Psi m) resulted in an increase of protein levels of cytochrome c, Apaf-1, caspase-9 and -3 in TSGH-8301 cells following exposure to EGCG. Proteomic analysis revealed that EGCG affected the expression levels of various proteins, including HSP27, porin, tropomyosin 3 isoform 2, prohibitin and keratin 5, 14, 17 in TSGH-8301 cells. EGCG also suppressed AKT kinase activity and protein levels and also altered the expression levels of Bcl-2 family-related proteins such as Bcl-2, Bax, BAD and p-BAD. Based on the above findings, this study suggests that EGCG-provoked apoptotic death in TSGH-8301 cells is mediated through targeting AKT and HSP27 and modulating p-BAD, leading to activation of the intrinsic apoptotic pathway.en_US
dc.language.isoen_USzh_TW
dc.relationOncology Reports, Volume 26, Issue 4, Page(s) 939-947.en_US
dc.relation.isversionofOncol. Rep.en_US
dc.relation.uri10.3892/or.2011.1377en_US
dc.subjectproteomicsen_US
dc.subjectepigallocatechin-3-gallateen_US
dc.subjectapoptosisen_US
dc.subjecthuman bladder canceren_US
dc.subjectTSGH-8301 cellsen_US
dc.subjectHSP27en_US
dc.subjectAKTen_US
dc.subjectintrinsic apoptotic signalingen_US
dc.subjectgreen-tea polyphenolen_US
dc.subjectbreast-cancer cellsen_US
dc.subjectinhibits tubulinen_US
dc.subjectpolymerizationen_US
dc.subjectcurcumin induces apoptosisen_US
dc.subjectbcl-2 family proteinsen_US
dc.subjectleukemiaen_US
dc.titleProteomic approaches to study epigallocatechin gallate-provoked apoptosis of TSGH-8301 human urinary bladder carcinoma cells: Roles of AKT and heat shock protein 27-modulated intrinsic apoptotic pathwaysen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.3892/or.2011.1377zh_TW
dc.contributor.catalogerMiao-zhen Luoen_US
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