Met overexpression confers HGF-dependent invasive phenotype to human thyroid carcinoma cells in vitro

Annarita De Luca, Niccolò Arena, Luigi M. Sena, Enzo Medico

Research output: Contribution to journalArticlepeer-review

Abstract

The proto-oncogene c-MET encodes the tyrosine kinase receptor for hepatocyte growth factor (HGF), a pleiotropic cytokine controlling growth, survival, motility, invasive migration, and differentiation of epithelial cells. Like several other epithelial neoplasms, thyroid carcinomas have been found to overexpress c-MET at both the mRNA and protein level. The biological relevance of Met overexpression to thyroid carcinoma natural history, however, remains to be elucidated. Therefore, we analyzed Met expression and response to HGF in two cell lines established from human thyroid carcinomas. In both lines we observed that the overexpressed ana constitutively tyrosine phosphorylated HGF receptor maintained biochemical responsiveness to the ligand. Both cell lines were also found to respond to HGF by consistently increasing their motility and invading in vitro reconstituted basal membranes. Conversely, no effect of HGF could be observed in proliferation and survival assays. These data show that overexpression of Met specifically confers to transformed thyroid cells a motile-invasive phenotype that is dependent on exogenous HGF stimulation.

Original languageEnglish
Pages (from-to)365-371
Number of pages7
JournalJournal of Cellular Physiology
Volume180
Issue number3
DOIs
Publication statusPublished - 1999

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

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