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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 >  Blockade of v-Src-stimulated tumor formation by the Src homology 3 domain of Crk-associated substrate (Cas)

Please use this identifier to cite or link to this item: http://nchuir.lib.nchu.edu.tw/handle/309270000/130704

標題: Blockade of v-Src-stimulated tumor formation by the Src homology 3 domain of Crk-associated substrate (Cas)
作者: Cheng, C.H.;Yu, K.C.;Chen, H.L.;Chen, S.Y.;Huang, C.H.;Chan, P.C.;Wung, C.W.;Chen, H.C.
陳鴻震
關鍵字: Src;Crk-associated substrate;Src homology 3 domain;tumor;anoikis;invasion;focal adhesion kinase;cell-migration;induced apoptosis;tyrosine;kinase;direct binding;p130(cas);protein;transformation;survival;growth
日期: 2004
Issue Date: 2012-12-07 16:05:44 (UTC+8)
關連: Febs Letters, Volume 557, Issue 1-3, Page(s) 221-227.
摘要: Crk-associated substrate (Cas) is highly phosphorylated by v-Src and plays a critical role in v-Src-induced cell transformation. In this study, we found that the Src homology (SH) 3 domain of Cas blocked v-Src-stimulated anchorage-independent cell growth, Matrigel invasion, and tumor growth in nude mice. Biochemical analysis revealed that the Cas SH3 domain selectively inhibited v-Src-stimulated activations of AKT and JNK, but not ERK and STAT3. Attenuation of the AKT pathway by the Cas SH3 domain rendered v-Src-transformed cells susceptible to apoptosis. Inhibition of the JNK pathway by the Cas SH3 domain led to suppression of v-Src-stimulated invasion. Taken together, our results indicate that the Cas SH3 domain has an anti-tumor function, which severely impairs the transforming potential of v-Src. (C) 2003 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Relation: Febs Letters
Appears in Collections:[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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