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因子 VIIa 通过 PAR2/MAPKs/NF-κB 信号通路调节 SW620 结肠癌细胞中 caspase-3、MMP-9 和 CD44 的表达。

Factor VIIa regulates the expression of caspase-3, MMP-9, and CD44 in SW620 colon cancer cells involving PAR2/MAPKs/NF-κB signaling pathways.

机构信息

Department of Internal Medicine, Affiliated Hospital of Jiangsu University, Jiangsu, PR China.

出版信息

Cancer Invest. 2013 Jan;31(1):7-16. doi: 10.3109/07357907.2012.743556. Epub 2012 Nov 21.

DOI:10.3109/07357907.2012.743556
PMID:23170789
Abstract

Our previous study has demonstrated that TF/FVIIa and PAR2 are closely related to the proliferation and migration of colon cancer cell line SW620. However, the detailed molecular mechanisms in the process remain unclear. This study further investigated whether some important molecules (caspase-3, MMP-9 and CD44) are involved in the events. The results showed that PAR2-AP or FVIIa elicited time-dependent downregulation of caspase-3, and up-regulation of MMP-9 and CD44 in SW620 cells. The effects of FVIIa were TF-dependent and involving PAR2/MAPKs/NF-κB signal transduction pathways. Our study suggests that the links among PAR2/MAPKs/NF-κB may be blocked for effective treatments of colorectal cancers.

摘要

我们之前的研究表明,TF/FVIIa 和 PAR2 与结肠癌细胞系 SW620 的增殖和迁移密切相关。然而,这一过程中的详细分子机制尚不清楚。本研究进一步探讨了一些重要分子(caspase-3、MMP-9 和 CD44)是否参与了这一过程。结果表明,PAR2-AP 或 FVIIa 可引起 SW620 细胞中 caspase-3 的时间依赖性下调和 MMP-9 和 CD44 的上调。FVIIa 的作用依赖于 TF,并涉及 PAR2/MAPKs/NF-κB 信号转导途径。我们的研究表明,PAR2/MAPKs/NF-κB 之间的联系可能被阻断,从而为结直肠癌的有效治疗提供可能。

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