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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.
Highlights
Laryngeal squamous cell carcinoma (LSCC) is one of the most common head and neck squamous cell carcinomas (HNSCC), and arises from the larynx epithelium with high metastasis rates and poor prognosis [1, 2]
Flow cytometry assay results showed that tumor Hep2 (T-Hep2) cells cultured with 0.1% Fetal Bovine Serum (FBS) for 48 h were in mainly G0/G1 phase (P
CoIP assay demonstrated the E2F4-P130 complex, unique in quiescent cells, in T-Hep2 cells cultured with 0.1% FBS for 48 h (Figure 1E)
Summary
Laryngeal squamous cell carcinoma (LSCC) is one of the most common head and neck squamous cell carcinomas (HNSCC), and arises from the larynx epithelium with high metastasis rates and poor prognosis [1, 2]. While treatment prolongs patient survival, metastatic tumor growth severely reduces overall survival rates [4, 5]. Elucidating the mechanisms of LSCC metastasis will be essential for identifying potential molecular targets to improve patient survival and quality of life. LSCC patients may develop local remnant or disseminated tumors. This phenomenon can be explained by tumor dormancy, a stage in tumor progression in which residual disease is present, but asymptomatic [6]. Mechanisms of tumor dormancy regulation are still largely unclear
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