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

3D mitochondria illustration used for peer reviewed papers on epicatechin and cellular energy research

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 charac-
terized 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 path-
ways, resulting in the inhibition of cell proliferation. Additionally, we found an increase in the sur-
vival 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 ef-
fects may occur through the modulation of deregulated AMPK and Akt/mTOR signalling pathways.