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题名: Autocrine CCL2 promotes cell migration and invasion via PKC activation and tyrosine phosphorylation of paxillin in bladder cancer cells
作者: Hsiao-Ying Chiu
Kuang-Hui Sun
Shiow-Yi Chen
Hsiao-Hsien Wang
Ming-Yung Lee
Yu-Chi Tsou
Shyh-Chuan Jwo
Guang-Huan Sun
Shye-Jye Tang
贡献者: 國立臺灣海洋大學:生命科學暨生物科技學系
关键词: Cell migration
MCP-1/CCL2
Bladder cancer
Paxillin
PKC
日期: 2012
上传时间: 2016-09-01T05:57:39Z
出版者: Cytokine
摘要: Abstract: The amount of monocyte chemoattractant protein-1 (MCP-1/CCL2) produced by a transitional cell carcinoma is directly correlated with high recurrence and poor prognosis in bladder cancer. However, the mechanisms underlying the effects of CCL2 on tumor progression remain unexplored. To investigate the role played by CCL2, we examined cell migration in various bladder cancer cell lines. We found that high-grade cancer cells expressing high levels of CCL2 showed more migration activity than low-grade bladder cancer cells expressing low levels of the chemokine. Although the activation of CCL2/CCR2 signals did not appreciably affect cell growth, it mediated cell migration and invasion via the activation of protein kinase C and phosphorylation of tyrosine in paxillin. Blocking CCL2 and CCR2 with small hairpin RNA (shCCL2) or a specific inhibitor reduced CCL2/CCR2-mediated cell migration. The antagonist of CCR2 promoted the survival of mice bearing MBT2 bladder cancer cells, and CCL2-depleted cells showed low tumorigenicity compared with shGFP cells. In addition to observing high-levels of CCL2 in high-grade human bladder cancer cells, we showed that the CCL2/CCR2 signaling pathway mediated migratory and invasive activity, whereas blocking the pathway decreased migration and invasion. In conclusion, high levels of CCL2 expressed in bladder cancer mediates tumor invasion and is involved with advanced tumorigenesis. Our findings suggest that this CCL2/CCR2 pathway is a potential candidate for the attenuation of bladder cancer metastases.
關聯: 59(2)
URI: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/38430
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