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National Chung Hsing University Institutional Repository - NCHUIR > 生命科學院 > 生命科學院 > 依資料類型分類 > 期刊論文 >  Functional suppression of E-cadherin by protein kinase C delta

Please use this identifier to cite or link to this item: http://nchuir.lib.nchu.edu.tw/handle/309270000/130719

標題: Functional suppression of E-cadherin by protein kinase C delta
作者: Chen, C.L.;Chen, H.C.
陳鴻震
關鍵字: PKCd;E-cadherin;Adherens junction;Tight junction;prostate-cancer cells;pkc-delta;epithelial-cells;junction;permeability;tumor promotion;activation;phosphorylation;adducin;actin;expression
日期: 2009
Issue Date: 2012-12-07 16:06:04 (UTC+8)
關連: Journal of Cell Science, Volume 122, Issue 4, Page(s) 513-523.
摘要: Protein kinase C (PKC) delta, a member of the novel PKC subfamily, has been shown to have an important role in cell proliferation, differentiation, apoptosis and cell motility. In this study, we investigated the effect of green fluorescent protein (GFP)-PKC delta and GFP-PKC alpha on cell-cell junctions of Madin-Darby canine kidney (MDCK) cells and found that only GFP-PKC delta suppressed the homophilic interactions between the ectodomains of E-cadherins, accompanied by a weaker cell-cell adhesion. The kinase-deficient mutant of GFP-PKC delta retained its localization at cell-cell junctions but failed to suppress the function of E-cadherin. In addition, we demonstrated that the hinge region (residues 280-347) that links the regulatory domain and the catalytic domain of PKC delta is essential for both its kinase activity and the targeting of cell-cell junctions. A PKCd mutant with the deletion of amino acids 280-323 within the hinge region, which is catalytically active but defective in the targeting of cell-cell junctions, failed to suppress the function of E-cadherin. Moreover, expression of GFP-PKC delta in MDCK cells expedited the detachment of cells from their neighbors and facilitated cell scatter induced by hepatocyte growth factor. By contrast, the GFP-PKC delta mutants including the kinase-deficient mutant and the truncated mutant lacking residues 280-323 suppressed hepatocyte-growth-factor-induced cell scattering. Finally, siRNA-mediated knockdown of endogenous PKC delta in MDCK cells was found to delay the onset of cell-cell detachment and cell scattering induced by hepatocyte growth factor. Taken together, our results demonstrate that the catalytic activity of PKCd and its localization to cell-cell junctions are necessary for PKCd to suppress the function of E-cadherin, which thereby facilitates scattering of epithelial cells in response to extracellular cues.
Relation: Journal of Cell Science
Appears in Collections:[依教師分類] 陳正倫
[依資料類型分類] 期刊論文
[依教師分類] 陳鴻震
[依教師分類] 陳鴻震

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