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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 >  Differential effect of the focal adhesion kinase Y397F mutant on v-Src-stimulated cell invasion and tumor growth

Please use this identifier to cite or link to this item: http://nchuir.lib.nchu.edu.tw/handle/309270000/130715

標題: Differential effect of the focal adhesion kinase Y397F mutant on v-Src-stimulated cell invasion and tumor growth
作者: Chang, L.C.;Huang, C.H.;Cheng, C.H.;Chen, B.H.;Chen, H.C.
關鍵字: anoikis;cell transformation;FAK;invasion;v-Src;protein-tyrosine kinase;jun nh2-terminal kinase;canine kidney-cells;phosphatidylinositol 3-kinase;anchorage independence;stable;association;induced apoptosis;family kinases;direct binding;in-vivo
日期: 2005
Issue Date: 2012-12-07 16:05:59 (UTC+8)
關連: Journal of Biomedical Science, Volume 12, Issue 4, Page(s) 571-585.
摘要: Upon cell adhesion to extracellular matrix proteins, focal adhesion kinase (FAK) rapidly undergoes autophosphorylation on its Tyr-397 which consequently serves as a binding site for the Src homology 2 domains of the Src family protein kinases and several other intracellular signaling molecules. In this study, we have attempted to examine the effect of the FAK Y397F mutant on v- Src- stimulated cell transformation by establishing an inducible expression of the Y397F mutant in v-Src-transformed FAK-null (FAK(-/-)) mouse embryo fibroblasts. We found that the FAK Y397F mutant had both positive and negative effects on v- Src- stimulated cell transformation; it promoted v- Src- stimulated invasion, but on the other hand it inhibited the v-Src-stimulated anchorage-independent cell growth in vitro and tumor formation in vivo. The positive e. ect of the Y397F mutant on v-Src- stimulated invasion was correlated with an increased expression of matrix metalloproteinase-2, both of which were inhibited by the specific phosphatidylinositol 3-kinase inhibitor wortmannin or a dominant negative mutant of AKT, suggesting a critical role for the phosphatidylinositol 3-kinase/AKT pathway in both events. However, the expression of the Y397F mutant rendered v- Src- transformed FAK(-/-) cells susceptible to anoikis, correlated with suppression on v-Src-stimulated activation of ERK and AKT. In addition, under anoikis stress, the induction of the Y397F mutant in v- Src- transformed FAK(-/-) cells selectively led to a decrease in the level of p130(Cas), but not other focal adhesion proteins such as talin, vinculin, and paxillin. These results suggest that FAK may increase the susceptibility of v- Src- transformed cells to anoikis by modulating the level of p130(Cas).
Relation: Journal of Biomedical Science
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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