AURKA promotes cell migration and invasion of head and neck squamous cell carcinoma through regulation of the AURKA/Akt/FAK signaling pathway | Zendy

Jichang Wu | Zendy; Liyun Yang | Zendy; Yamin Shan | Zendy; Changping Cai | Zendy; Shili Wang | Zendy; Hao Zhang | Zendy

Open Access

AURKA promotes cell migration and invasion of head and neck squamous cell carcinoma through regulation of the AURKA/Akt/FAK signaling pathway

Author(s) -

Jichang Wu,

Liyun Yang,

Yamin Shan,

Changping Cai,

Shili Wang,

Hao Zhang

Publication year - 2016

Publication title -

oncology letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.766

H-Index - 54

eISSN - 1792-1082

pISSN - 1792-1074

DOI - 10.3892/ol.2016.4110

Subject(s) - protein kinase b , focal adhesion , head and neck squamous cell carcinoma , cancer research , cell migration , signal transduction , phosphorylation , cell , cell cycle , cell growth , kinase , chemistry , biology , microbiology and biotechnology , medicine , cancer , head and neck cancer , biochemistry

The present study aimed to investigate the mechanism by which Aurora kinase A (AURKA) promotes cell migration and invasion in head and neck squamous cell carcinoma (HNSCC). Transwell assays were performed to investigate the cell migration and invasion abilities of AURKA, whilst western blotting was used to analyze the protein expression in FaDu and Hep2 cells, each treated with pharmacological inhibitors. Following the inhibition of AURKA, Akt and focal adhesion kinase (FAK), the migration and invasion of the FaDu and Hep2 cells decreased. The expression of phosphorylated (p)-AURKA and p-FAK (Y397) was observed to decrease following FaDu and Hep2 cell treatment with VX-680, a small molecular inhibitor of AURKA. The expression of p-Akt and p-FAK (Y397) ceased following treatment with the Akt inhibitor triciribine. The expression of p-FAK (Y397) decreased, however, p-Akt expression did not change following treatment with the FAK inhibitor TAE226. In conclusion, AURKA activates FAK through the AURKA/Akt/FAK signaling pathway, promoting the migration and invasion of HNSCC cells, which may subsequently provide a novel approach for the treatment of HNSCC.

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