[E-cadherin affects MAP activation by growth factors stimulation in human carcinoma cells].
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.
Bagaeva
V V
VV
Avrov
K A
KA
Reshetnikova
G F
GF
D015820:Cadherins / Q000502:physiology*; D002448:Cell Adhesion; D045744:Cell Line, Tumor; D002465:Cell Movement; D003600:Cytosol / Q000378:metabolism; D066246:ErbB Receptors / Q000378:metabolism; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D006801:Humans; D007365:Intercellular Junctions / Q000378:metabolism; D019859:Proto-Oncogene Proteins c-met / Q000378:metabolism; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism*; D015398:Signal Transduction
D015820:Cadherins; D066246:ErbB Receptors; D048049:Extracellular Signal-Regulated MAP Kinases; D019859:Proto-Oncogene Proteins c-met; D018719:Erb-b2 Receptor Tyrosine Kinases