Inhibition of Estradiol Receptor/Src Association and Cell Growth by an Estradiol Receptor {alpha} Tyrosine-Phosphorylated Peptide.

Inhibition of Estradiol Receptor/Src Association and Cell Growth by an Estradiol Receptor {alpha} Tyrosine-Phosphorylated Peptide. Research Abstract Details 

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Inhibition of Estradiol Receptor/Src Association and Cell Growth by an Estradiol Receptor {alpha} Tyrosine-Phosphorylated Peptide. Abstract Text:

Lilian Varricchio,Antimo Migliaccio,Gabriella Castoria,Hiroshi Yamaguchi,Antonietta de Falco,Marina Di Domenico,Pia Giovannelli,William Farrar,Ettore Appella,Ferdinando Auricchio,Lilian Varricchio,Antimo Migliaccio,Gabriella Castoria,Hiroshi Yamaguchi,Antonietta de Falco,Marina Di Domenico,Pia Giovannelli,William Farrar,Ettore Appella,Ferdinando Auricchio,Lilian Varricchio,Antimo Migliaccio,Gabriella Castoria,Hiroshi Yamaguchi,Antonietta de Falco,Marina Di Domenico,Pia Giovannelli,William Farrar,Ettore Appella,Ferdinando Auricchio,

This report offers direct evidence that association of the estradiol receptor (ER) with Src triggered by steroid agonists or growth factors controls breast and prostate cancer cell growth. This association is abolished in whole cells and in vitro by a six-amino-acid peptide that mimics the sequence around the phosphotyrosine residue in position 537 of the human ERalpha. The phosphorylated peptide, at nanomolar concentrations, is taken up by MCF-7 and LNCaP cells derived from human mammary and prostate cancers, respectively. In addition, to block the ER/Src interaction, the phosphopeptide inhibits Src/Erk pathway, cyclin D1 expression, and DNA synthesis induced by estradiol or androgen or triggered by epidermal growth factor. In contrast, no inhibition of the Src-mediated epidermal growth factor action on DNA synthesis is detectable in human mammary cancer cells that do not express ER (MDA-MB231), indicating that the peptide specifically targets the ER-associated Src. Remarkably, the peptide, in contrast with classic steroid antagonists, does not interfere in ER- or androgen receptor-dependent transcriptional activity. Nevertheless, it markedly inhibits the growth of MCF-7 cell xenografts induced in immunodepressed and estradiol-treated mice. The present report suggests that inhibition of association of steroid receptors with Src or other signaling effectors may have therapeutic applications for patients with ER-positive tumors. (Mol Cancer Res 2007;5(11):1213-21).

Inhibition of Estradiol Receptor/Src Association and Cell Growth by an Estradiol Receptor {alpha} Tyrosine-Phosphorylated Peptide. Publishing Authors By Initials

L Varricchio,A Migliaccio,G Castoria,H Yamaguchi,A de Falco,M Di Domenico,P Giovannelli,W Farrar,E Appella,F Auricchio,L Varricchio,A Migliaccio,G Castoria,H Yamaguchi,A de Falco,M Di Domenico,P Giovannelli,W Farrar,E Appella,F Auricchio,L Varricchio,A Migliaccio,G Castoria,H Yamaguchi,A de Falco,M Di Domenico,P Giovannelli,W Farrar,E Appella,F Auricchio,

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Inhibition of Estradiol Receptor/Src Association and Cell Growth by an Estradiol Receptor {alpha} Tyrosine-Phosphorylated Peptide. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Molecular cancer research : MCR

VOLUME: 5

Page Numbers: 1213-21

Journal Abbreviation: Mol. Cancer Res.

ISSN: 1541-7786

DAY: 20

MONTH: Nov

YEAR: 2007

Inhibition of Estradiol Receptor/Src Association and Cell Growth by an Estradiol Receptor {alpha} Tyrosine-Phosphorylated Peptide. Information

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LANGUAGE: eng

NlmUniqueID: 101150042

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AFFILIATION: Department of General Pathology, II University of Naples, Via L. De Crecchio, 7, Naples 80138, Italy. ferdinando.auricchio@unina2.it.

Country: United States

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MEDLINETA: Mol Cancer Res

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