E-CADHERIN AFFECTS MAP ACTIVATION BY GROWTH FACTORS STIMULATION IN HUMAN CARCINOMA CELLS
V. V. Bagaeva, K. A. Avrov, G. F. Reshetnikova 1
Institute of Cytology RAS, St. Petersburg;
1 e-mail: greshet@mail.cytspb.rssi.ru
Met and EGF receptor (EGFR) activation is correlated with dissociation of cell-cell adhesion and with increase
in mobility of cancer cells. E-cadherin is a major protein of adhesion junctions. Using different approaches
we have shown that EGF receptors intracellular localization depends of E-cadherin function. It was found that
EGFR localized on the membrane in HT-29 cells which formed mature cell-cell contacts. Moreover, EGFR was
colocalized with E-cadherin at the site of cell-cell adhesion in Triton-insoluble fraction. EGFR was accumulated
preliminary in cytosol in E-cadherin negative HBL-100 cells. Study of signal transduction mediated by EGF and
HGF in cells with different state of cell adhesion demonstrated that E-cadherin could affect ERK-signal-duration.
Our preliminary studies proposed that mislocalization of Met and EGFR in E-cadherin negative cells altered
receptors downstream signaling.
Key words: Met, EGF receptor, E-cadherin, cell-cell adhesion, MAP kinase
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