Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 정낙신 | - |
dc.date.accessioned | 2018-05-30T08:14:04Z | - |
dc.date.available | 2018-05-30T08:14:04Z | - |
dc.date.issued | 2006 | - |
dc.identifier.issn | 1535-7163 | - |
dc.identifier.other | OAK-3258 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/243497 | - |
dc.description.abstract | Agonists to A3 adenosine receptor (A3AR) have been reported to inhibit cell growth and/or induce apoptosis in various tumors. We tested the effect of a novel A3AR agonist generically known as LJ-529 in breast cancer cells. Anchorage-dependent cell growth and in vivo tumor growth were attenuated by LJ-529, independently of its estrogen receptor (ER) α status. In addition, apoptosis was induced as evidenced by the activation of caspase-3 and c-poly(ADP)ribose polymerase. Furthermore, the Wnt signaling pathway was down-regulated and p27kip was induced by LJ-529. In ER-positive cells, the expression of ER was down-regulated by LJ-529, which might have additionally contributed to attenuated cell proliferation. In ER-negative, c-ErbB2-overexpressing SK-BR-3 cells, the expression of c-ErbB2 and its downstream extracellular signal-regulated kinase pathway were down-regulated by LJ-529. However, such effect of LJ-529 acted independently of its receptor because no A3AR was detected by reverse transcription-PCR in all four cell lines tested. In conclusion, our novel findings open the possibility of LJ-529 as an effective therapeutic agent against both ER-positive and ER-negative breast cancers, particularly against the more aggressive ER-negative, c-ErbB2-overexpressing types. Copyright © 2006 American Association for Cancer Research. | - |
dc.language | English | - |
dc.title | The antitumor effect of LJ-529, a novel agonist to A3 adenosine receptor, in both estrogen receptor-positive and estrogen receptor-negative human breast cancers | - |
dc.type | Article | - |
dc.relation.issue | 3 | - |
dc.relation.volume | 5 | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 685 | - |
dc.relation.lastpage | 692 | - |
dc.relation.journaltitle | Molecular Cancer Therapeutics | - |
dc.identifier.doi | 10.1158/1535-7163.MCT-05-0245 | - |
dc.identifier.wosid | WOS:000236444500024 | - |
dc.identifier.scopusid | 2-s2.0-33645472346 | - |
dc.author.google | Chung H. | - |
dc.author.google | Jung J.-Y. | - |
dc.author.google | Cho S.-D. | - |
dc.author.google | Hong K.-A. | - |
dc.author.google | Kim H.-J. | - |
dc.author.google | Shin D.-H. | - |
dc.author.google | Kim H. | - |
dc.author.google | Kim H.O. | - |
dc.author.google | Shin D.H. | - |
dc.author.google | Lee H.W. | - |
dc.author.google | Jeong L.S. | - |
dc.author.google | Kong G. | - |
dc.contributor.scopusid | 정낙신(16028528200) | - |
dc.date.modifydate | 20211210153610 | - |