Alisertib promotes apoptosis and autophagy in melanoma through p38 MAPK-mediated aurora a signaling.

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Alisertib promotes apoptosis and autophagy in melanoma through p38 MAPK-mediated aurora a signaling.

Oncotarget. 2017 Dec 05;8(63):107076-107088

Authors: Shang YY, Yao M, Zhou ZW, Jian-Cui, Li-Xia, Hu RY, Yu YY, Qiong-Gao, Biao-Yang, Liu YX, Dang J, Zhou SF, Nan-Yu

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.

PMID: 29291012 [PubMed]

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