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dc.contributor.authorAltiok N.
dc.contributor.authorKoyuturk M.
dc.contributor.authorAltiok S.
dc.date.accessioned2019-08-13T12:10:23Z
dc.date.accessioned2019-08-13T15:53:39Z
dc.date.available2019-08-13T12:10:23Z
dc.date.available2019-08-13T15:53:39Z
dc.date.issued2007
dc.identifier.issn0167-6806
dc.identifier.urihttps://dx.doi.org/10.1007/s10549-006-9451-1
dc.identifier.urihttp://hdl.handle.net/11446/1990
dc.descriptionPubMed ID: 17187235en_US
dc.description.abstractEstrogen is known to stimulate breast cancer development in humans. Ironically, high doses of estrogen can induce regression of hormone-dependent breast cancer in postmenopausal women. The mechanism by which estrogen induces tumour regression in breast cancer is still unknown. We found that under low growth-stimulated conditions, high concentrations of 17-?-estradiol (estradiol) induces apoptosis and concomitantly increases phosphorylation of c-jun in estrogen receptor (ER)-positive breast cancer cell line, MCF-7, but not in ER-negative breast cancer cell line MDA-MB 231 suggesting an ER-mediated event. Interestingly, when the c-jun NH2-terminal kinase (JNK) signalling pathway was disrupted by the JNK inhibitor SP600125, the ability of estradiol to inhibit the growth of MCF-7 cells and to induce apoptosis was completely blocked. These data suggest that JNK plays a central role in mediating the anticancer effect of high concentrations of estradiol in MCF-7 cells. Our data showing the apoptotic effect of estradiol in low growth-stimulated conditions suggest potential implications for the pharmacological control of breast cancer with high dose estrogen in postmenopausal women. Furthermore, our results indicate that augmenting JNK activity could be an efficient novel approach for treating breast cancer. © 2006 Springer Science+Business Media, LLC.en_US
dc.description.sponsorshipJohns Hopkins University Brain Science Institute, Johns Hopkins Universityen_US
dc.description.sponsorshipAcknowledgements This study was supported by Istanbul Science University Institute of Medical Sciences and Johns Hopkins University Institutional research grant.en_US
dc.language.isoengen_US
dc.relation.isversionof10.1007/s10549-006-9451-1en_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApoptosisen_US
dc.subjectBreast canceren_US
dc.subjectEstradiolen_US
dc.subjectJNKen_US
dc.subjectTUNELen_US
dc.titleJNK pathway regulates estradiol-induced apoptosis in hormone-dependent human breast cancer cellsen_US
dc.typearticleen_US
dc.relation.journalBreast Cancer Research and Treatmenten_US
dc.contributor.departmentDBÜen_US
dc.identifier.issue3en_US
dc.identifier.volume105en_US
dc.identifier.startpage247en_US
dc.identifier.endpage254en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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