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J Pharm Pharmacol ; 73(12): 1675-1682, 2021 Dec 07.
Artigo em Inglês | MEDLINE | ID: mdl-34473289

RESUMO

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.


Assuntos
Antineoplásicos Fitogênicos/farmacologia , Catequina/farmacologia , Glândulas Mamárias Humanas/metabolismo , Fitoterapia , Extratos Vegetais/farmacologia , Neoplasias de Mama Triplo Negativas/metabolismo , Proteínas Quinases Ativadas por AMP/metabolismo , Animais , Antineoplásicos Fitogênicos/uso terapêutico , Catequina/uso terapêutico , Linhagem Celular Tumoral , Proliferação de Células , Doxorrubicina/farmacologia , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Camundongos Endogâmicos BALB C , Fosforilação , Extratos Vegetais/uso terapêutico , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Serina-Treonina Quinases TOR/metabolismo , Neoplasias de Mama Triplo Negativas/tratamento farmacológico
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