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Characterization of a novel negative regulator (DOC-2/DAB2) of c-Src in normal prostatic epithelium and cancer.

Authors: Zhou, J  Scholes, J  Hsieh, JT 
Citation: Zhou J, etal., J Biol Chem. 2003 Feb 28;278(9):6936-41. Epub 2002 Dec 8.
Pubmed: (View Article at PubMed) PMID:12473651
DOI: Full-text: DOI:10.1074/jbc.M210628200

DOC-2/DAB2 is a potent tumor suppressor in many cancer types including prostate cancer. In prostate cancer, expression of DOC-2/DAB2 can inhibit its growth. Our recent studies demonstrate that DOC-2/DAB2 can suppress both protein kinase C and peptide growth factor-elicited signal pathways via the Ras-mitogen-activated protein kinase pathway. In this study, we further showed that the proline-rich domain of DOC-2/DAB2 could also interact with proteins containing the Src homology 3 domain, such as Src and Fgr. The binding of c-Src to DOC-2/DAB2 was enhanced in cells treated with growth factor, and this interaction resulted in c-Src inactivation. The c-Src inactivation was evidenced by the decreased tyrosine 416 phosphorylation of c-Src and reduced downstream effector activation. It appears that DOC-2/DAB2 can bind to Src homology 3 domain of c-Src and maintain it in an inactive conformation. Thus, this study provides a new mechanism for modulating c-Src in prostatic epithelium and cancer.

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CRRD Object Information
CRRD ID: 8553624
Created: 2014-05-08
Species: All species
Last Modified: 2014-05-08
Status: ACTIVE



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