Open Access

ARTICLE

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

Ruoyu Wang^*†, Heming Li^†, Xuefen Guo^†, Zhe Wang^†, Shanshan Liang^†, Chengxue Dang^*

* Department of Surgical Oncology, The First Affiliated Hospital, Xi’an Jiaotong University College of Medicine, Xi’an, P.R. China
† Department of Oncology, Zhongshan Hospital of Dalian University, Dalian, P.R. China

Oncology Research 2016, 24(4), 225-231. https://doi.org/10.3727/096504016X14648701447931

Abstract

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-Iinduced 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.

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