AI Article Synopsis
- The study explored how Alisertib (ALS), which inhibits Aurora kinase A, affects melanoma cells.
- ALS was found to slow down cell growth (anti-proliferative), promote cell death (pro-apoptotic), and enhance cell degradation processes (pro-autophagic) by blocking p38 MAPK signaling.
- Further findings showed that combining ALS with a specific p38 MAPK inhibitor boosted the effectiveness of ALS, suggesting that ALS could be a promising treatment for melanoma.
Article 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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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5739797 | PMC |
| http://dx.doi.org/10.18632/oncotarget.22328 | DOI Listing |
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