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• W2021921749 abstract "A hallmark of transforming growth factorβ (TGFβ) action is the induction of the synthesis and secretion of extracellular-matrix adhesion molecules and induction of the cell-surface expression of integrin receptors for these molecules (termed extracellular-matrix remodeling). The signal pathways leading to extracellular-matrix remodeling and the significance of extracellular-matrix remodeling in TGFβ function is not well-understood. In the epithelium-derived human colon cancer cell line Moser, TGFβ induces extracellular-matrix remodeling in a protein kinase Cα-dependent manner. In this study we showed that TGFβ was a potent inducer of the homotypic cell–cell adhesion molecule E-cadherin and its undercoat-associated proteins, the catenins and dramatically increased the amount of E-cadherin/γ-catenin complex formation. We found that the induction of E-cadherin and α- and β-catenin by TGFβ was also dependent on protein kinase Cα, whereas the induction of γ-catenin was independent of protein kinase Cα but dependent on other protein kinase C isoforms. We also found that protein kinase Cα-dependent induction of extracellular-matrix remodeling and subsequent cell–matrix interaction requiring both fibronectin and laminin were a prerequisite for the induction of E-cadherin (and α- and β-catenin but not γ-catenin) by TGFβ. We therefore concluded that two signal pathways exist in TGFβ-regulated expression of E-cadherin and the catenins. We also concluded that a functional significance of TGFβ-induced extracellular matrix remodeling is the activation of signal transduction mechanisms through increased interaction between extracellular matrix fibronectin and laminin and their cell-surface integrin receptors, which lead to the induction of E-cadherin (and α- and β-catenin). © 2001 Wiley-Liss, Inc." @default.
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• W2021921749 date "2001-01-01" @default.
• W2021921749 modified "2023-09-23" @default.
• W2021921749 title "Requirement of protein kinase C?, extracellular matrix remodeling, and cell-matrix interaction for transforming growth factor?-regulated expression of E-cadherin and catenins" @default.
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• W2021921749 doi "https://doi.org/10.1002/jcp.1068" @default.
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