Publication:
Involvement of ERK1/2 in Invasiveness and Metastatic Development of Rat Prostatic Adenocarcinoma

dc.contributor.authorTuangporn Suthiphongchaien_US
dc.contributor.authorPiradee Promyarten_US
dc.contributor.authorSariya Virochruten_US
dc.contributor.authorRutaiwan Tohtongen_US
dc.contributor.authorPrapon Wilairaten_US
dc.contributor.otherMahidol Universityen_US
dc.date.accessioned2018-07-24T02:56:03Z
dc.date.available2018-07-24T02:56:03Z
dc.date.issued2002-12-01en_US
dc.description.abstractExtracellular signal-regulated kinase (ERK) activation has been implicated in cell motility and invasion. In this study, we demonstrated that the steady-state levels of activated ERK1/2 correlated with the degree of invasiveness and metastatic potential of three Dunning cancer cell lines, originating from the same parental tumor. Inhibition of mitogen-activated protein kinase kinase 1 (MEK1), an upstream regulator of ERK1/2, with PD98059 resulted in a dose-dependent reduction of invasiveness with different IC 50 values in the three Dunning cell lines. These results suggest that ERK is, at least in part, responsible for regulating invasiveness and may underlie the differences in the metastatic ability of the cell lines.en_US
dc.identifier.citationOncology Research. Vol.13, No.5 (2002), 253-259en_US
dc.identifier.issn09650407en_US
dc.identifier.other2-s2.0-0141889542en_US
dc.identifier.urihttps://repository.li.mahidol.ac.th/handle/123456789/20016
dc.rightsMahidol Universityen_US
dc.rights.holderSCOPUSen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0141889542&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleInvolvement of ERK1/2 in Invasiveness and Metastatic Development of Rat Prostatic Adenocarcinomaen_US
dc.typeArticleen_US
dspace.entity.typePublication
mu.datasource.scopushttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0141889542&origin=inwarden_US

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