NLRP3 inflammasome-mediated cytokine production and pyroptosis cell death in breast cancer.

Fiche publication

Date publication

avril 2021

Journal

Journal of biomedical science

Auteurs

Membres identifiés du Cancéropôle Est :
Dr RIALLAND Mickaël

Tous les auteurs :
Faria SS, Costantini S, de Lima VCC, de Andrade VP, Rialland M, Cedric R, Budillon A, Magalhães KG

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/33840390

Résumé

Breast cancer is the most diagnosed malignancy in women. Increasing evidence has highlighted the importance of chronic inflammation at the local and/or systemic level in breast cancer pathobiology, influencing its progression, metastatic potential and therapeutic outcome by altering the tumor immune microenvironment. These processes are mediated by a variety of cytokines, chemokines and growth factors that exert their biological functions either locally or distantly. Inflammasomes are protein signaling complexes that form in response to damage- and pathogen-associated molecular patterns (DAMPS and PAMPS), triggering the release of pro-inflammatory cytokines. The dysregulation of inflammasome activation can lead to the development of inflammatory diseases, neurodegeneration, and cancer. A crucial signaling pathway leading to acute and chronic inflammation occurs through the activation of NLRP3 inflammasome followed by caspase 1-dependent release of IL-1β and IL-18 pro-inflammatory cytokines, as well as, by gasdermin D-mediated pyroptotic cell death. In this review we focus on the role of NLRP3 inflammasome and its components in breast cancer signaling, highlighting that a more detailed understanding of the clinical relevance of these pathways could significantly contribute to the development of novel therapeutic strategies for breast cancer.