Activation of the FAK/PI3K pathway is crucial for AURKA-induced epithelial-mesenchymal transition in laryngeal cancer

作者：Yang, Liyun; Zhou, Quan; Chen, Xuehua; Su, Liping; Liu, Bingya; Zhang, Hao^*

来源：Oncology Reports, 2016, 36(2): 819-826.

DOI：10.3892/or.2016.4872

• laryngeal cancer
• AURKA
• epithelial-mesenchymal transition
• FAK/PI3K pathway
• metastasis

Laryngeal squamous cell carcinoma (LSCC) is one of the most common malignant tumors, and the main cause of death is metastasis. Overexpression of aurora kinase A (AURKA) plays an important role in the metastasis of LSCC. However, the mechanism by which AURKA promotes the metastasis of LSCC is poorly understood. Recent accumulating evidence indicates that epithelial-mesenchymal transition (EMT) may be one of the mechanisms of tumor metastasis. In the present study, we studied whether AURKA may induce EMT to promote the metastasis of LSCC. CCK-8 and plate colony-formation assays were carried out to show that AURKA significantly promoted the proliferation of Hep2 cells. Immunofluorescence staining and western blotting showed that EMT-related proteins changed in a time-dependent manner along with the alteration of AURKA, with decreased expression of N-cadherin, vimentin and slug and increased expression of E-cadherin. Additionally, downregulation of the expression of AURKA inhibited FAK/PI3K pathway activity. Inhibition of the FAK/PI3K pathway caused less mesenchymal-like characteristics and reduced the mobility, migration and invasion of Hep2 cells. In conclusion, AURKA may induce EMT to promote metastasis via activation of the FAK/PI3K pathway in LSCC. Those regulatory factors may present new diagnostic biomarkers and potential therapeutic targets for LSCC.

• 出版日期2016-8
• 单位上海交通大学; 上海市闵行区中心医院