首页> 外文期刊>Journal of biochemical and molecular toxicology >Focal Adhesion Kinase Knockdown in Carcinoma-Associated Fibroblasts Inhibits Oral Squamous Cell Carcinoma Metastasis via Downregulating MCP-1/CCL2 Expression
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Focal Adhesion Kinase Knockdown in Carcinoma-Associated Fibroblasts Inhibits Oral Squamous Cell Carcinoma Metastasis via Downregulating MCP-1/CCL2 Expression

机译:癌相关的成纤维细胞中的黏着斑激酶基因敲低通过下调MCP-1 / CCL2表达抑制口腔鳞状细胞癌转移。

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Carcinoma-associated fibroblasts (CAFs) have been demonstrated to play an important role in the occurrence and development of oral squamous cell carcinoma (OSCC). The aim of this study is to investigate the influence of CAFs on OSCC cells and to explore the role of focal adhesion kinase (FAK) in this process. The results showed that oral CAFs expressed a higher level of FAK than normal human gingival fibroblasts (HGFs), and the conditioned medium (CM) of CAFs could induce the invasion and migration of SCC-25, one oral squamous carcinoma cell line. However, knockdown of FAK by small interfering RNA (siRNA) resulted in inhibition of CAF-CM induced cell invasion and migration in SCC-25, probably by reducing the production of monocyte chemoattractant protein-1 (MCP-1/CCL2), one of downstream target chemokines. Therefore, our findings indicated that targeting FAK in CAFs might be a promising strategy for the treatment of OSCC in the future. (C) 2014 Wiley Periodicals, Inc.
机译:癌相关的成纤维细胞(CAF)已被证明在口腔鳞状细胞癌(OSCC)的发生和发展中起着重要作用。这项研究的目的是调查CAF对OSCC细胞的影响,并探讨粘着斑激酶(FAK)在此过程中的作用。结果表明,口服CAFs表达的FAK水平高于正常人牙龈成纤维细胞(HGFs),并且CAFs的条件培养基(CM)可以诱导SCC-25(一种口腔鳞状细胞癌细胞系)的侵袭和迁移。但是,通过小干扰RNA(siRNA)抑制FAK可能会抑制CAF-CM诱导的SCC-25细胞侵袭和迁移,可能是通过减少单核细胞趋化蛋白1(MCP-1 / CCL2)的产生来实现的。下游目标趋化因子。因此,我们的发现表明,在CAF中靶向FAK可能是将来治疗OSCC的有前途的策略。 (C)2014威利期刊公司

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