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

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.
Mesh Terms:
Adaptor Proteins, Signal Transducing, Adaptor Proteins, Vesicular Transport, Animals, COS Cells, Enzyme Activation, Enzyme Inhibitors, Genes, Tumor Suppressor, Glutathione Transferase, Humans, Male, Mitogen-Activated Protein Kinases, Models, Biological, Mutation, Peptides, Phosphorylation, Precipitin Tests, Prostate, Prostatic Neoplasms, Protein Binding, Protein Biosynthesis, Protein Conformation, Protein Kinase C, Protein Structure, Tertiary, Protein-Tyrosine Kinases, Recombinant Fusion Proteins, Signal Transduction, Time Factors, Transfection, Tumor Cells, Cultured, Tyrosine
J. Biol. Chem.
Date: Feb. 28, 2003
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