Breast tumor kinase and extracellular signal-regulated kinase 5 mediate Met receptor signaling to cell migration in breast cancer cells |
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| Authors: | Nancy E Castro and Carol A Lange |
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| Affiliation: | (1) Department of Pharmacology, University of Minnesota, 321 Church Street S.E., Minneapolis, MN 55455, USA;(2) Department of Medicine (Division of Hematology, Oncology, and Transplantation), University of Minnesota, MN 55455, 420 Delaware Street S.E., Minneapolis, MN 55455, USA;(3) Masonic Cancer Center, University of Minnesota, MN 55455, 425 E. River Road, Minneapolis, MN 55455, USA |
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| Abstract: | Introduction Breast tumor kinase (Brk/protein tyrosine kinase 6 (PTK6)) is a nonreceptor, soluble tyrosine kinase overexpressed in the majority of breast tumors. Previous work has placed Brk downstream of epidermal growth factor receptor (ErbB) activation and upstream of extracellular signal-regulated kinase 5 (ERK5) and p38 mitogen-activated protein (MAP) kinases. Herein we investigate the regulation of Brk kinase activity and cell migration in response to treatment of keratinocytes (HaCaT cells) and breast cancer cell lines (MDA-MB-231 and T47D cells) with hepatocyte growth factor (HGF) and macrophage stimulating protein (MSP), peptide ligands for Met and Ron receptors, respectively. |
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