Mechanisms of HGF/Met Signaling to Brk and Sam68 in Breast Cancer Progression

Alessia Locatelli, Kristopher A. Lofgren, Andrea R. Daniel, Nancy E. Castro, Carol A. Lange

Research output: Contribution to journalReview articlepeer-review

32 Scopus citations

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 languageEnglish (US)
Pages (from-to)14-25
Number of pages12
JournalHormones and Cancer
Volume3
Issue number1-2
DOIs
StatePublished - 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

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