IGF-I Induces Epithelial-to-Mesenchymal Transition via the IGF-IR-Src-MicroRNA-30a-E-Cadherin Pathway in Nasopharyngeal Carcinoma Cells.
IGF-I Induces Epithelial-to-Mesenchymal Transition via the IGF-IR-Src-MicroRNA-30a-E-Cadherin Pathway in Nasopharyngeal Carcinoma Cells.
复制标题
IGF-I 在鼻咽癌细胞中通过 IGF-IR-Src MicroRNA-30a-E-钙粘蛋白途径诱导上皮细胞向间质细胞的转变
DOI：
10.3727/096504016x14648701447931
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发表时间：
2016
影响因子：
3.1
通讯作者：
Dang C
中科院分区：
文献类型：
--
作者：
Wang R;Li H;Guo X;Wang Z;Liang S;Dang C
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.
