Definition of a direct extracellular interaction between Met and E-cadherin

Galina Reshetnikova*, Sergei Troyanovsky, David L. Rimm

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


High levels of the Met tyrosine kinase receptor expression are associated with metastatic disease. Met activation by hepatocyte growth factor (HGF) is associated with decreased E-cadherin-dependent cell-cell contacts. The molecular mechanism underlying this process remains unclear. To better understand the relationship between E-cadherin and Met, we assessed Met localization in cells which form mature E-cadherin-dependent adhesion HT-29 and cells which have lost E-cadherin expression BT-549. Met colocalized with E-cadherin at the site of cell-cell adhesion in HT-29 cells, but Met was distributed in an intracellular compartment in BT-549 cells. Forced expression of E-cadherin in BT-549 cells recruited Met to the membrane. Cross-linking studies suggested that Met and E-cadherin interact in the extracellular domain in HT-29 cells. This is the first evidence of a physical interaction between Met and E-cadherin. We suggest that this receptor/cadherin pairing may be a mechanism for cellular presentation of receptors in a manner that localizes them optimally for interaction with ligand.

Original languageEnglish (US)
Pages (from-to)366-373
Number of pages8
JournalCell Biology International
Issue number4 SPEC. ISS.
StatePublished - Apr 2007


  • E-cadherin
  • Hepatocyte growth factor
  • Met
  • Receptor tyrosine kinase

ASJC Scopus subject areas

  • Cell Biology


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