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dc.contributor.authorChaiwat Prawettongsoponen_US
dc.contributor.authorSariya Asawakarnen_US
dc.contributor.authorTuangporn Suthiphongchaien_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherChulalongkorn Universityen_US
dc.date.accessioned2018-09-13T06:20:45Z-
dc.date.available2018-09-13T06:20:45Z-
dc.date.issued2009-12-08en_US
dc.identifier.citationOncology Research. Vol.17, No.7 (2009), 301-309en_US
dc.identifier.issn09650407en_US
dc.identifier.other2-s2.0-65649089560en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=65649089560&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/27098-
dc.description.abstractUpregulation of the PI3K pathway has often been reported in androgen-independent prostate cancer and is implicated in cancer cell survival and proliferation in the absence of androgen. Inhibition of PI3K by LY294002 suppressed cell invasion and motility of the highly metastatic androgen-independent Dunning rat prostate cancer MLL cell line with similar IC50 values and inhibition profile. Moreover, LY294002 attenuated expression of urokinase plasminogen activator (uPA) without any significant effect on that of matrix metalloproteinase 2. These results indicated that the role of PI3K in MLL cell invasion is by regulating cell motility and uPA expression. Copyright © 2009 Cognizant Comm. Corp. All rights reseved.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=65649089560&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectMedicineen_US
dc.titleSuppression of prometastatic phenotype of highly metastatic androgen-independent rat prostate cancer MLL cell line by PI3K inhibitor LY294002en_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.3727/096504009787721195en_US
Appears in Collections:Scopus 2006-2010

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