Research Papers:
Alisertib promotes apoptosis and autophagy in melanoma through p38 MAPK-mediated aurora a signaling
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Abstract
Yuan-Yuan Shang1,2,*, Ming Yao3,2,*, Zhi-Wei Zhou2, Jian-Cui4, Li-Xia1, Rong-Ying Hu1, Ying-Yao Yu1, Qiong-Gao1, Biao-Yang1, Yu-Xi Liu1, Jie Dang5, Shu-Feng Zhou2 and Nan-Yu1
1Department of Dermatology, General Hospital of NingXia Medical University, Yinchuan, P.R. China
2Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA
3Department of Burns and Plastic Surgery, General Hospital of NingXia Medical University, Yinchuan, P.R. China
4Department of Anesthesia, General Hospital of NingXia Medical University, Yinchuan, P.R. China
5Department of Medical Genetics and Cell Biology, Ningxia Medical University, Yinchuan, P.R.China
*These authors have contributed equally to this work
Correspondence to:
Shu-Feng Zhou, email: [email protected]
Nan-Yu, email: [email protected]
Keywords: alisertib; melanoma; AURKA; MAPK
Received: June 06, 2017 Accepted: September 21, 2017 Published: November 06, 2017
ABSTRACT
We investigated the efficacy of Alisertib (ALS), a selective Aurora kinase A (AURKA) inhibitor, in melanoma. We found that ALS exerts anti-proliferative, pro-apoptotic, and pro-autophagic effects on A375 and skmel-5 melanoma cells by inhibiting p38 MAPK signaling. SB202190, a p38 MAPK-selective inhibitor, enhanced ALS-induced apoptosis and autophagy in both cell lines. ALS induced cell cycle arrest in melanoma cells through activation of the p53/p21/cyclin B1 pathway. Knockdown of p38 MAPK enhanced ALS-induced apoptosis and reduced ALS-induced autophagy. Inhibition of autophagy sensitized melanoma cells to ALS-induced apoptosis. These data indicate ALS is a potential therapeutic agent for melanoma.
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