Brk/PTK6 signaling in normal and cancer cell models

Julie H Ostrander, Andrea R. Daniel, Carol A Lange

Research output: Contribution to journalReview articlepeer-review

48 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)662-669
Number of pages8
JournalCurrent Opinion in Pharmacology
Volume10
Issue number6
DOIs
StatePublished - Dec 2010

Bibliographical note

Funding Information:
We would like to thank Ming Qiu for technical support. This work was supported by NIH R01 CA107547-01 (CAL), ACS Research Scholar Award RSG TBE-107800 (CAL), and National Research Service Award 1F32CA112844-01A2 (JHO).

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