Myogenic microRNAs as Therapeutic Targets for Skeletal Muscle Mass Wasting in Breast Cancer Models

Autor(es)

Artigas-Arias, Macarena ; Curi, Rui ; Marzuca-Nassr, Gabriel Nasri

• Tipo de documento: Artigo Científico
• Fonte: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES; v. 25, n. 12, p. 16-pg., 2024-06-01.

Resumo

Breast cancer is the type of cancer with the highest prevalence in women worldwide. Skeletal muscle atrophy is an important prognostic factor in women diagnosed with breast cancer. This atrophy stems from disrupted skeletal muscle homeostasis, triggered by diminished anabolic signalling and heightened inflammatory conditions, culminating in an upregulation of skeletal muscle proteolysis gene expression. The importance of delving into research on modulators of skeletal muscle atrophy, such as microRNAs (miRNAs), which play a crucial role in regulating cellular signalling pathways involved in skeletal muscle protein synthesis and degradation, has been recognised. This holds true for conditions of homeostasis as well as pathologies like cancer. However, the determination of specific miRNAs that modulate skeletal muscle atrophy in breast cancer conditions has not yet been explored. In this narrative review, we aim to identify miRNAs that could directly or indirectly influence skeletal muscle atrophy in breast cancer models to gain an updated perspective on potential therapeutic targets that could be modulated through resistance exercise training, aiming to mitigate the loss of skeletal muscle mass in breast cancer patients. (AU)

• Processo FAPESP: 18/09868-7 - Mecanismos celulares e moleculares envolvidos na resistência à insulina e inflamação em ratos Wistar obesos e Goto-Kakizaki magros: causas e associações com dieta e exercício físico
• Beneficiário: Rui Curi
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 22/09341-4 - Pré-habilitação baseada no treinamento resistido em mulheres com Câncer de Mama em terapia neoadjuvante: do mecanismo molecular aos benefícios clínicos
• Beneficiário: Rui Curi
• Modalidade de apoio: Auxílio à Pesquisa - Regular