Abstract
Signal transduction pathways downstream of receptor tyrosine kinases (RTKs) are often deregulated during oncogenesis, tumor progression, and metastasis. In particular, the peptide growth factor hormone, hepatocyte growth factor (HGF), and its specific receptor, Met tyrosine kinase, regulate cancer cell migration, thereby conferring an aggressive phenotype (Nakamura et al., J Clin Invest 106(12):1511-1519, 2000; Huh et al., Proc Natl Acad Sci U S A 101:4477-4482, 2004). Additionally, overexpression of Met is associated with enhanced invasiveness of breast cancer cells (Edakuni et al., Pathol Int 51(3):172-178, 2001; Jin et al., Cancer 79(4):749-760, 1997; Tuck et al., Am J Pathol 148(1):225-232, 1996). Here, we review the regulation of recently identified novel downstream mediators of HGF/Met signaling, Breast tumor kinase (Brk/PTK6), and Src-associated substrate during mitosis of 68 kDa (Sam68), and discuss their relevance to mechanisms of breast cancer progression.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 14-25 |
| Number of pages | 12 |
| Journal | Hormones and Cancer |
| Volume | 3 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Apr 2012 |
Bibliographical note
Funding Information:Acknowledgements Work in Carol A. Lange Laboratory was supported by American Cancer Society RSG TBE-107800 (to CAL) and NIH/NCI grant CA107547 (to CAL). We thank Dr. Gwen Dressing for helpful comments.
Keywords
- Breast cancer
- Brk
- Cell migration
- Erk5
- HGF
- Met
- PTK6
- Sam68
