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IGF-I Induces Epithelial-to-Mesenchymal Transition via the IGF-IR-Src MicroRNA-30a-E-Cadherin Pathway in Nasopharyngeal Carcinoma Cells

机译:IGF-I通过鼻咽癌细胞中的IGF-IR-Src MicroRNA-30a-E-钙黏着蛋白途径诱导上皮向间充质转化。

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摘要

Recurrence and distant metastasis are the most common cause of therapeutic failure in nasopharyngeal carcinoma (NPC) patients. Insulin-like growth factor I (IGF-I) can induce epithelial-to-mesenchymal transition (EMT) in many epithelial tumors; however, whether IGF-I can enhance NPC metastasis by EMT and the mechanisms remain unclear. Herein, we have identified that IGF-I could induce EMT and enhance migration ability in NPC cell lines. Furthermore, both Src inhibitor and microRNA-30a (miR-30a) inhibitor reversed IGF-I-induced EMT, suggesting the involvement of an IGF-IR Src miR-30a E-cadherin pathway in IGF-I-induced EMT in NPC cell lines. Overall, the results of the present study may provide more useful information regarding the mechanisms of the IGF-IR signaling pathway in the regulation of NPC metastasis. Both Src kinase and miR-30a can be potential biomarkers for selecting high risk of metastasis in NPC patients.
机译:复发和远处转移是鼻咽癌(NPC)患者治疗失败的最常见原因。胰岛素样生长因子I(IGF-1)可以在许多上皮肿瘤中诱导上皮向间质转化(EMT)。但是,IGF-I是否可以通过EMT增强NPC转移,其机制尚不清楚。在本文中,我们已经鉴定出IGF-1可以诱导EMT并增强NPC细胞系中的迁移能力。此外,Src抑制剂和microRNA-30a(miR-30a)抑制剂均逆转了IGF-I诱导的EMT,表明IGF-IR Src miR-30a E-钙粘蛋白途径参与了NPC细胞系IGF-I诱导的EMT。 。总体而言,本研究的结果可能会提供有关IGF-IR信号传导途径调控NPC转移的更多有用信息。 Src激酶和miR-30a均可作为潜在的生物标记物,用于选择NPC患者的高转移风险。

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