Department of Microbiology, Immunology, and Molecular Genetics, Molecular Biology Institute, Department of Obstetrics and Gynecology, and The David Geffen School of Medicine, Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, and The Howard Hughes Medical Institute, University of California, Los Angeles, CA 90095.
Src family kinases (SFKs) are pleiotropic activators that are responsible for integrating signal transduction for multiple receptors that regulate cellular proliferation, invasion, and metastasis in a variety of human cancers. Independent groups have identified increased expression of individual SFK members during prostate cancer progression, raising the question of whether SFKs display functional equivalence. Here, we show that Src kinase, followed by Fyn kinase and then Lyn kinase, exhibit ranked tumorigenic potential during both paracrine-induced and cell-autonomous-initiated prostate cancer. This quantitative variation in transformation potential appears to be regulated in part by posttranslational palmitoylation. Our data indicate that development of inhibitors against specific SFK members could provide unique targeted therapeutic strategies.
Written by:
Cai H, Smith DA, Memarzadeh S, Lowell CA, Cooper JA, Witte ON. Are you the author?
Reference: Proc Natl Acad Sci U S A. 2011 Apr 19;108(16):6579-84.
doi: 10.1073/pnas.1103904108
PubMed Abstract
PMID: 21464326
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