Abstract
Knowledge of the molecular events that contribute to prostate cancer progression has created opportunities to develop novel therapy strategies. It is now well established that c-Src, a non-receptor tyrosine kinase, regulates a complex signaling network that drives the development of castrate-resistance and bone metastases, events that signal the lethal phenotype of advanced disease. Preclinical studies have established a role for c-Src and Src Family Kinases (SFKs) in proliferation, angiogenesis, invasion and bone metabolism, thus implicating Src signaling in both epithelial and stromal mechanisms of disease progression. A number of small molecule inhibitors of SFK now exist, many of which have demonstrated efficacy in preclinical models and several that have been tested in patients with metastatic castrate-resistant prostate cancer. These agents have demonstrated provocative clinic activity, particularly in modulating the bone microenvironment in a therapeutically favorable manner. Here, we review the discovery and basic biology of c-Src and further discuss the role of SFK inhibitors in the treatment of advanced prostate cancer.
Original language | English (US) |
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Pages (from-to) | 595-606 |
Number of pages | 12 |
Journal | Cancer and Metastasis Reviews |
Volume | 33 |
Issue number | 2-3 |
DOIs | |
State | Published - Sep 2014 |
Keywords
- Dasatinib
- Prostate cancer
- SFK inhibitors
- Src
ASJC Scopus subject areas
- Oncology
- Cancer Research