Anticancer potential of (−)-epicatechin in a triple-negative mammary gland model

Author:

Almaguer Georgina1,Ortiz-Vilchis Pilar1,Cordero Paola1,Martinez-Vega Rocío1,Perez-Durán Javier12,Meaney Eduardo1,Villarreal Francisco3,Ceballos Guillermo1ORCID,Nájera Nayelli1ORCID

Affiliation:

1. Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, México City, México

2. Department of Human Genetics and Genomics, Instituto Nacional de Perinatología, Mexico City, Mexico

3. Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA

Abstract

Abstract Objectives The main aim of this work was to analyse the potential tumour growth inhibition effects of (−)-epicatechin (EC). Triple-negative breast cancer (TNBC) is an invasive form of cancer characterized by the absence of progesterone receptor, estrogen receptor and human epidermal growth factor receptor 2. Doxorubicin (DOX) is widely used for its anti-tumour activity. EC belongs to the flavanol subfamily and is a candidate molecule for the adjuvant treatment of cancer due to its antiproliferative activities. Methods Evaluation of EC effects and pathways involved in a model of TNBC. Key findings EC inhibited tumour growth as efficiently as DOX (inhibition rates of 74% and 79% for EC and DOX, respectively). The evaluation of adenosine monophosphate-activated protein kinase (AMPK) and Akt phosphorylation and mTOR expression indicates that EC modulates these pathways, resulting in the inhibition of cell proliferation. Additionally, we found an increase in the survival of EC-treated animals compared with control-treated animals. This effect was similar to the effects induced by DOX (survival rates of 44% and 30% for EC and DOX, respectively). Conclusion EC has antiproliferative properties and increases survival in a model of TNBC. These effects may occur through the modulation of deregulated AMPK and Akt/mTOR signalling pathways.

Funder

National Institutes of Health

Publisher

Oxford University Press (OUP)

Subject

Pharmaceutical Science,Pharmacology

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