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Autophagy regulates Selumetinib (AZD6244) induced-apoptosis in colorectal cancer cells

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Date
2016
Author
Grasso, Silvina [UNIFESP]
Pereira, Gustavo José da Silva [UNIFESP]
Santos, Caroline Palmeira dos [UNIFESP]
Calgarotto, Andrana Karla [UNIFESP]
Martinez-Lacaci, Isabel
Antonio Ferragut, Jose
Smaili, Soraya Soubhi [UNIFESP]
Bincoletto, Claudia [UNIFESP]
Type
Artigo
ISSN
0223-5234
Is part of
European Journal Of Medicinal Chemistry
DOI
10.1016/j.ejmech.2016.06.043
Metadata
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Abstract
Objective: As Selumetinib is a MEK1/2 inhibitor that has gained interest as an anti-tumor agent, the present study was designed to investigate autophagy involvement on Selumetinib-induced apoptosis in colorectal cancer (CRC) cells. Methods: CRC cells death and cycle studies were assessed by AnnexinV-FITC and PI staining, respectively. Autophagy flux was analysed by Western Blot (LC3II and p62 protein levels) and retroviral infection of SW480 cells for siBecn1 RNA interference experiments. Confocal microscopy was used to determine mCherry-EGFP-LC3 distribution. Key findings: The Selumetinib effects were concentration-dependent in SW480 cell line. Whereas 1 mu M exerted an arrest in the cell cycle (G1 phase), higher concentrations (10 mu M) induced cell death, which was accompanied by autophagy blockage in its last stages. Autophagy induction by Rapamycin (RAPA) increased cell survival, whereas pharmacology autophagy inhibition by Bafilomycin A1 (BAF), Chloroquine (CQ) or 3-Methyladenine (3-MA) increased Selumetinib-induced CRC cells death. Conclusions: Altogether, these results suggest that autophagy plays a fundamental role in CRC cells response to Selumetinib. In addition, the combination of Selumetinib with autophagy inhibitors may be a useful therapeutic strategy to enhance its activity against colorectal tumours. (C) 2016 Elsevier Masson SAS. All rights reserved.
Citation
European Journal Of Medicinal Chemistry. Paris, v. 122, p. 611-618, 2016.
Keywords
Apoptosis
Autophagy
Selumetinib (AZD6244)
CRC cells (SW480 and HT29)
Sponsorship
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
URI
https://repositorio.unifesp.br/handle/11600/56888
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  • EPM - Artigos [17701]

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