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Am J Cancer Res. 2015 Feb 15;5(3):1133-45. eCollection 2015.

Inhibition of Aurora A promotes chemosensitivity via inducing cell cycle arrest and apoptosis in cervical cancer cells.

Author information

1
Cancer Institute, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Gynecological Oncology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Department of Obstetrics and Gynecology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine Shanghai 200062, China.
2
Cancer Institute, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China.
3
Department of Breast Oncology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China.
4
Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Department of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China.
5
Department of Gynecological Oncology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China.
6
Cancer Institute, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Central Laboratory, The Fifth People's Hospital of Shanghai, Fudan University Shanghai 200240, China.

Abstract

Aurora kinase A (AurA) regulates genomic instability and tumorigenesis in multiple cancer types. Although some studies have reported that Aur A may predict cervical cancer outcomes, its precise function and molecular mechanism in cervical cancer pathogenesis remain unclear. In this study, by overexpression or silencing of Aur A in cervical cancer cell lines, we found that overexpression of Aur A promoted cell proliferation through G1/S cell cycle transition and anti-apoptosis, xenograft tumor growth and chemoresistance to Taxol. We further found that inhibition of Aur A with its specific inhibitor VX-680 enhanced the antitumor effect of Taxol via inducing apoptosis. Moreover, the clinical analysis from tissue samples demonstrated that Aur A was overexpressed, and the expression of Aur A and pERK1/2 was negatively correlated in cervical cancer tissues. The above results may provide some potential insights in treatment of cervical cancer in clinic.

KEYWORDS:

Aurora A; Taxol; VX-680; cervical cancer; chemoresistance

PMID:
26045992
PMCID:
PMC4449441

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