TY - JOUR
T1 - Anticancer potential of (−)-epicatechin in a triple-negative mammary gland model
AU - Almaguer, Georgina
AU - Ortiz-Vilchis, Pilar
AU - Cordero, Paola
AU - Martinez-Vega, Rocío
AU - Perez-Durán, Javier
AU - Meaney, Eduardo
AU - Villarreal, Francisco
AU - Ceballos, Guillermo
AU - Nájera, Nayelli
N1 - Publisher Copyright:
© The Author(s) 2021. Published by Oxford University Press on behalf of the Royal Pharmaceutical Society. All rights reserved.
PY - 2021/12/1
Y1 - 2021/12/1
N2 - 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.
AB - 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.
KW - epicatechin
KW - mammary gland
KW - survival
KW - tumour
UR - http://www.scopus.com/inward/record.url?scp=85122500885&partnerID=8YFLogxK
U2 - 10.1093/jpp/rgab133
DO - 10.1093/jpp/rgab133
M3 - Artículo
C2 - 34473289
AN - SCOPUS:85122500885
SN - 0022-3573
VL - 73
SP - 1675
EP - 1682
JO - Journal of Pharmacy and Pharmacology
JF - Journal of Pharmacy and Pharmacology
IS - 12
ER -