Oncotarget

Research Papers:

Aurora kinase A revives dormant laryngeal squamous cell carcinoma cells via FAK/PI3K/Akt pathway activation

Li-yun Yang, Chang-yu He, Xue-hua Chen, Li-ping Su, Bing-ya Liu and Hao Zhang _

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Oncotarget. 2016; 7:48346-48359. https://doi.org/10.18632/oncotarget.10233

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Abstract

Li-yun Yang1, Chang-yu He2, Xue-hua Chen2, Li-ping Su2, Bing-ya Liu2, Hao Zhang1

1Department of Otolaryngology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China

2Shanghai Key Laboratory of Gastric Neoplasms, Shanghai Institute of Digestive Surgery, School of Medicine, Shanghai Jiaotong University, Shanghai, China

Correspondence to:

Hao Zhang, email: [email protected]

Keywords: laryngeal cancer, aurora kinase A, FAK, PI3K, Akt

Received: December 29, 2015     Accepted: June 09, 2016     Published: June 23, 2016

ABSTRACT

Revival of dormant tumor cells may be an important tumor metastasis mechanism. We hypothesized that aurora kinase A (AURKA), a cell cycle control kinase, promotes the transition of laryngeal squamous cell carcinoma (LSCC) cells from G0 phase to active division. We therefore investigated whether AURKA could revive dormant tumor cells to promote metastasis. Western blotting revealed that AURKA expression was persistently low in dormant laryngeal cancer Hep2 (D-Hep2) cells and high in non-dormant (T-Hep2) cells. Decreasing AURKA expression in T-Hep2 cells induced dormancy and reduced FAK/PI3K/Akt pathway activity. Increasing AURKA expression in D-Hep2 cells increased FAK/PI3K/Akt pathway activity and enhanced cellular proliferation, migration, invasion and metastasis. In addition, FAK/PI3K/Akt pathway inhibition caused dormancy-like behavior and reduced cellular mobility, migration and invasion. We conclude that AURKA may revive dormant tumor cells via FAK/PI3K/Akt pathway activation, thereby promoting migration and invasion in laryngeal cancer. AURKA/FAK/PI3K/Akt inhibitors may thus represent potential targets for clinical LSCC treatment.


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