Inhibition of E-Cadherin Dependent Cell-Cell Contact Promotes MUC5AC Mucin Production through the Activation of Epidermal Growth Factor Receptors

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  • IWASHITA Jun
    Molecular Biology Laboratory, Faculty of Bioresource Sciences, Akita Prefectural University
  • OSE Kyohei
    Molecular Biology Laboratory, Faculty of Bioresource Sciences, Akita Prefectural University
  • ITO Hiroki
    Molecular Biology Laboratory, Faculty of Bioresource Sciences, Akita Prefectural University
  • MURATA Jun
    Molecular Biology Laboratory, Faculty of Bioresource Sciences, Akita Prefectural University
  • ABE Tatsuya
    Molecular Biology Laboratory, Faculty of Bioresource Sciences, Akita Prefectural University

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Mucin production by epithelial cells is modulated by many soluble factors, including epidermal growth factor (EGF). E-Cadherin promotes EGF receptor (EGFR)-mediated MUC5AC mucin production in airway epithelial cells in dense cultures, suggesting the involvement of E-cadherin in activating EGFRs and mucin production. However, the role of E-cadherin in modulating mucin production is not completely understood. We examined its role in MUC5AC production in a human lung epithelial cell line, NCI-H292. Treatment of low density NCI-H292 cells with an anti-E-cadherin monoclonal antibody (SHE78-7) inhibited cell-cell contact in the dispersed colonies, but promoted MUC5AC production. Furthermore, treatment of the NCI-H292 cells with anti-E-cadherin antibody stimulated phosphorylation of extracellular signal-regulated kinase (ERK). The enhanced production of MUC5AC was inhibited with an EGFR inhibitor and with a MEK inhibitor, but not with a Src family kinase inhibitor. These results suggest that inhibition of E-cadherin activates EGFRs independently of Src and promotes MUC5AC production through the ERK signaling pathway in sparsely cultured NCI-H292 cells.

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