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CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells

Breast cancer is the second leading cause of death amongst women worldwide. As a result, many have turned their attention to new alternative approaches to treat this disease. Caffeic acid phenylethyl ester (CAPE), a well-known active compound from bee propolis, has been previously identified as a st...

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Autores principales: Beauregard, Annie-Pier, Harquail, Jason, Lassalle-Claux, Grégoire, Belbraouet, Mehdi, Jean-Francois, Jacques, Touaibia, Mohamed, Robichaud, Gilles A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6332101/
https://www.ncbi.nlm.nih.gov/pubmed/26184141
http://dx.doi.org/10.3390/molecules200712576
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author Beauregard, Annie-Pier
Harquail, Jason
Lassalle-Claux, Grégoire
Belbraouet, Mehdi
Jean-Francois, Jacques
Touaibia, Mohamed
Robichaud, Gilles A.
author_facet Beauregard, Annie-Pier
Harquail, Jason
Lassalle-Claux, Grégoire
Belbraouet, Mehdi
Jean-Francois, Jacques
Touaibia, Mohamed
Robichaud, Gilles A.
author_sort Beauregard, Annie-Pier
collection PubMed
description Breast cancer is the second leading cause of death amongst women worldwide. As a result, many have turned their attention to new alternative approaches to treat this disease. Caffeic acid phenylethyl ester (CAPE), a well-known active compound from bee propolis, has been previously identified as a strong antioxidant, anti-inflammatory, antiviral and anticancer molecule. In fact, CAPE is well documented as inducing cell death by inhibiting NFκB and by inducing pro-apoptotic pathways (i.e., p53). With the objective of developing stronger anticancer compounds, we studied 18 recently described CAPE derivatives for their ability to induce apoptosis in breast cancer cell lines. Five of the said compounds, including CAPE, were selected and subsequently characterised for their anticancer mechanism of action. We validated that CAPE is a potent inducer of caspase-dependent apoptosis. Interestingly, some newly synthesized CAPE derivatives also showed greater cell death activity than the lead CAPE structure. Similarly to CAPE, analog compounds elicited p53 activation. Interestingly, one compound in particular, analog 10, induced apoptosis in a p53-mutated cell line. These results suggest that our new CAPE analog compounds may display the capacity to induce breast cancer apoptosis in a p53-dependent and/or independent manner. These CAPE analogs could thus provide new therapeutic approaches for patients with varying genotypic signatures (such as p53 mutations) in a more specific and targeted fashion.
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spelling pubmed-63321012019-01-24 CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells Beauregard, Annie-Pier Harquail, Jason Lassalle-Claux, Grégoire Belbraouet, Mehdi Jean-Francois, Jacques Touaibia, Mohamed Robichaud, Gilles A. Molecules Article Breast cancer is the second leading cause of death amongst women worldwide. As a result, many have turned their attention to new alternative approaches to treat this disease. Caffeic acid phenylethyl ester (CAPE), a well-known active compound from bee propolis, has been previously identified as a strong antioxidant, anti-inflammatory, antiviral and anticancer molecule. In fact, CAPE is well documented as inducing cell death by inhibiting NFκB and by inducing pro-apoptotic pathways (i.e., p53). With the objective of developing stronger anticancer compounds, we studied 18 recently described CAPE derivatives for their ability to induce apoptosis in breast cancer cell lines. Five of the said compounds, including CAPE, were selected and subsequently characterised for their anticancer mechanism of action. We validated that CAPE is a potent inducer of caspase-dependent apoptosis. Interestingly, some newly synthesized CAPE derivatives also showed greater cell death activity than the lead CAPE structure. Similarly to CAPE, analog compounds elicited p53 activation. Interestingly, one compound in particular, analog 10, induced apoptosis in a p53-mutated cell line. These results suggest that our new CAPE analog compounds may display the capacity to induce breast cancer apoptosis in a p53-dependent and/or independent manner. These CAPE analogs could thus provide new therapeutic approaches for patients with varying genotypic signatures (such as p53 mutations) in a more specific and targeted fashion. MDPI 2015-07-10 /pmc/articles/PMC6332101/ /pubmed/26184141 http://dx.doi.org/10.3390/molecules200712576 Text en © 2015 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Beauregard, Annie-Pier
Harquail, Jason
Lassalle-Claux, Grégoire
Belbraouet, Mehdi
Jean-Francois, Jacques
Touaibia, Mohamed
Robichaud, Gilles A.
CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells
title CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells
title_full CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells
title_fullStr CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells
title_full_unstemmed CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells
title_short CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells
title_sort cape analogs induce growth arrest and apoptosis in breast cancer cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6332101/
https://www.ncbi.nlm.nih.gov/pubmed/26184141
http://dx.doi.org/10.3390/molecules200712576
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