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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
- 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
- Authors
- Chung H.; Jung J.-Y.; Cho S.-D.; Hong K.-A.; Kim H.-J.; Shin D.-H.; Kim H.; Kim H.O.; Shin D.H.; Lee H.W.; Jeong L.S.; Kong G.
- Ewha Authors
- 정낙신
- SCOPUS Author ID
- 정낙신
- Issue Date
- 2006
- Journal Title
- Molecular Cancer Therapeutics
- ISSN
- 1535-7163
- Citation
- Molecular Cancer Therapeutics vol. 5, no. 3, pp. 685 - 692
- Indexed
- SCIE; SCOPUS
- Document Type
- Article
- 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.
- DOI
- 10.1158/1535-7163.MCT-05-0245
- Appears in Collections:
- 약학대학 > 약학과 > Journal papers
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