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KISS1 gene suppresses metastasis of nasopharyngeal cancer via activation of the ERK1/2 pathway

机译： KISS1 基因通过激活ERK1 / 2途径抑制鼻咽癌的转移

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Nasopharyngeal cancer (NPC) is one of the most common head and neck cancers in the world. The failure of the treatment of NPC is mainly caused by the metastasis of the cancer cells. There is a great need to study the mechanism of metastasis for accurate diagnosis, prognosis and efficient therapeutic strategy. The KISS1 gene has already been reported as a metastasis suppressor in numerous cancers. In this study, by integrating the Transwell assay, western blotting and real-time reverse transcriptase polymerase chain reaction (RT-PCR) analysis, we found that the expression of KISS1 and its receptor gene (hOT7T175, KISS1R) negatively related with the metastasis of NPC cells. Overexpression of the KISS1 and KISS1R genes reduced migration and invasion of the SUNE-1-5-8F cells that are a cell line of NPC. Additionally, overexpression of these genes significantly increased the phosphorylation of focal adhesion kinase (FAK) and decreased the expression of ezrin (EZR), indicated by western blotting. Further study showed the metastasis suppression role of KISS1 and KISS1R was mediated though phosphorylation of the ERK1/2 pathway for that blocking the phosphorylation of the pathway with inhibitor (PD98059) reversed the metastasis suppression and phosphorylation of FAK as well as up-regulation of EZR simultaneously. Together, all of these results suggested for the first time that KISS1 and KISS1R suppress the metastasis of NPC cells by phosphorylation of FAK and decreasing EZR through phosphorylation of the ERK1/2 pathway.
机译：鼻咽癌（NPC）是世界上最常见的头颈癌之一。鼻咽癌治疗失败的主要原因是癌细胞的转移。为了准确诊断，预后和有效治疗策略，迫切需要研究转移的机制。 KISS1 基因已被报道为多种癌症的转移抑制因子。在这项研究中，通过整合Transwell分析，蛋白质印迹和实时逆转录聚合酶链反应（RT-PCR）分析，我们发现 KISS1 及其受体基因（hOT7T175，< em> KISS1R ）与NPC细胞的转移负相关。 KISS1 和 KISS1R 基因的过表达减少了作为NPC细胞系的SUNE-1-5-8F细胞的迁移和侵袭。此外，这些蛋白的过表达显着增加了粘着斑激酶（FAK）的磷酸化，并降低了ezrin（EZR）的表达，这是通过Western blotting进行的。进一步的研究表明，尽管通过抑制ERK1 / 2途径的磷酸化来阻断 KISS1 和 KISS1R 的转移抑制作用，但用抑制剂（PD98059）阻断了该途径的磷酸化逆转了同时抑制FAK的转移和磷酸化以及EZR的上调。总之，所有这些结果首次提示 KISS1 和 KISS1R 通过FAK的磷酸化抑制NPC细胞的转移，并通过ERK1 / 2途径的磷酸化降低EZR 。

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