Caffeine Inhibits Migration in Glioma Cells through the ROCK-FAK Pathway

被引：26
作者：
Chen, Ying [1 ]
Chou, Wei-Chung [1 ]
Ding, You-Ming [1 ]
Wu, Ya-Chieh [2 ]
机构：
[1] Natl Def Med Ctr, Dept Biol & Anat, Taipei 114, Taiwan
[2] Ching Kuo Inst Management & Hlth, Dept Nursing, Keelung, Taiwan
来源：
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY | 2014年 / 33卷 / 06期
关键词：
Caffeine; Rho associated kinase; Focal adhesion kinase; Glioma; ADHESION; ACTIVATION; INVASION;
D O I：
10.1159/000362966
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Aims: Glioma is the most malignant brain tumor that has the ability to migrate and invade the CNS. In this study, we investigated the signaling mechanism of caffeine on the migration of glioma cells. Methods: The effect of caffeine on cell migration was evaluated using Transwell and wound healing assays. The expression of the focal adhesion complex as it related to cell migration was assayed using Western blotting and immunostaining. Results: Caffeine decreased the migration of rat C6 and human U87MG glioma cells and down-regulated the expression of phosphorylated focal adhesion kinase (p-FAK) and p-paxillin. Caffeine also decreased p-FAK staining at the edge of glioma cells and disassembled actin stress fibers. Additionally, caffeine elevated expression of phosphorylated myosin light chain (p-MLC), an effect that could be blocked by Y27632, a rho-associated protein kinase (ROCK) inhibitor, but not myosin light chain kinase inhibitor, ML-7. Y27632 also inhibited the caffeine reduced expression of p-FAK and p-paxillin as well as cell migration. Conclusion: Caffeine decreased the migration of glioma cell through the ROCK focal adhesion complex pathway; this mechanism may be useful as part of clinical therapy in the future. Copyright (C) 2014 S. Karger AG, Basel
引用
收藏
页码：1888 / 1898
页数：11
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