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首页> 外文期刊>Journal of Cellular Physiology >Inhibition of epidermal growth factor-induced invasion by dexamethasone and AP-1 decoy in human squamous cell carcinoma cell lines.
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Inhibition of epidermal growth factor-induced invasion by dexamethasone and AP-1 decoy in human squamous cell carcinoma cell lines.

机译：抑制表皮生长因素地塞米松和AP-1入侵人类的诱饵鳞状细胞癌细胞系。

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Invasive squamous cell carcinoma (SCC) cells degrade extracellular matrix (ECM) via an extracellular protease cascade that includes urokinase-type plasminogen activator (uPA), plasmin, and the metalloprotease (MMP) family of collagenases. In this study, treatment of oral SCC cells with epidermal growth factor (EGF) stimulated the cells to invade Matrigel (constructive basement membrane (BM) protein). EGF-induced cell invasion was inhibited by antibodies to uPA and by synthetic uPA inhibitors. EGF also induced increased expression of uPA and uPA receptor (uPAR) proteins and mRNA, as well as transcription factor activator protein-1 (AP-1)-DNA binding. These EGF-induced changes were inhibited by treatment with dexamethasone (DEX). DEX treatment also stimulated the production of plasminogen activator inhibitor type 1. Moreover, transfection of SCC cells with AP-1 decoy oligodeoxynucleotides (ODNs) resulted in the suppression of EGF-induced uPA and uPAR expression and Matrigel invasion. These results suggest that oral SCC cells invade Matrigel mainly through the uPA-plasmin cascade, which is mediated by the transcription factor AP-1. The uPA-uPAR interaction is essential for augmenting proteolytic activity and uPAR-mediated signaling, which ultimately induce motility and invasion. Since DEX inhibits the expression of both uPA and uPAR, it may be a useful treatment for oral SCC. J. Cell. Physiol. 193: 340-348, 2002. Copyright 2002 Wiley-Liss, Inc.
机译：浸润性鳞状细胞癌(SCC)细胞降解细胞外基质(ECM)通过一个包括细胞外蛋白酶级联urokinase-type纤溶酶原激活物(uPA),血纤维蛋白溶酶,metalloprotease (MMP)的家庭胶原酶。鳞状细胞癌细胞表皮生长因子(EGF)刺激细胞入侵基底膜基质(建设性的基底膜(BM)蛋白质)。EGF-induced细胞入侵被抑制合成uPA uPA和抗体抑制剂。uPA和uPA受体(uPAR)蛋白质和信使rna,以及转录因子激活dna结合蛋白1 (AP-1)。变化被治疗地塞米松(DEX)。刺激生产的纤溶酶原。物激活抑制剂1型。转染AP-1诱饵的鳞状细胞癌的细胞oligodeoxynucleotides (ODNs)导致抑制EGF-induced uPA和uPAR表达和基底膜基质入侵。表明口腔鳞状细胞癌基底膜基质细胞入侵主要通过uPA-plasmin级联,这是介导的转录因子AP-1。uPA-uPAR交互对增加至关重要蛋白水解活性和uPAR-mediated信号,最终引起能动性和入侵。因为敏捷抑制uPA和的表达uPAR,它可能是一个有用的治疗口腔鳞状细胞癌。j .细胞。2002 Wiley-Liss, Inc。

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