Journal
CURRENT OPINION IN PHARMACOLOGY
Volume 10, Issue 6, Pages 662-669Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2010.08.007
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Funding
- NIH [R01 CA107547 01]
- ACS [RSG TBE 107800]
- National Research Service Award [1F32CA112844 01A2]
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Breast tumor kinase (Brk) also termed PTK6 is known to function in cell-type and context-dependent processes governing normal differentiation However, in tumors in which Brk is overexpressed, this unusual soluble tyrosine kinase is emerging as a mediator of cancer cell phenotypes, including increased proliferation survival and migration Nuclear and cytoplasmic substrates phosphorylated by Brk include a collection of regulatory RNA-binding proteins, adaptor molecules that link Brk to signaling pathways generally associated with the activation of growth factor receptors, and Signal Transducers and Activators of Transcription (STAT) molecules that are direct regulators of gene expression Understanding Brk-dependent regulation of these key signaling pathways and how they influence cancer cell behavior is predicted to inform the development of improved targeted cancer therapies and may provide insight into ways to avoid chemo-resistance to established treatments
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