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Immunol Lett ; 232: 60-66, 2021 04.
Article in English | MEDLINE | ID: mdl-33647328

ABSTRACT

Breast cancer is a leading cause of death worldwide and a better understanding of this disease is needed to improve treatment outcomes. Recent evidence indicates that bacterial dysbiosis is associated with breast cancer, but the bacteria involved remain poorly characterised. Furthermore, an association between periodontal disease, characterised by oral dysbiosis, and breast cancer have also been discovered, but the mechanisms responsible for this association remains to be elucidated. The oral bacterium involved in periodontal disease, Fusobacterium nucleatum, have recently been detected in human breast tumour tissue and it promoted tumour growth and metastatic progression in a mouse model. The mechanisms of how F. nucleatum might colonise breast tissue and how it might promote tumour progression has not been fully elucidated yet. Here we discuss the breast tumour microbiota, its colonisation by F. nucleatum, possible mechanisms by which F. nucleatum might promote breast cancer progression and how this might impact breast cancer treatment. Literature indicates that F. nucleatum might promote breast cancer progression through activating the Toll-like receptor 4 pathway and by supressing the immune system. This results in cell growth and treatment resistance through autophagy as well as immune evasion. Targeted treatment directed at F. nucleatum combined with immunotherapy and autophagy inhibitors might therefore be a feasible treatment strategy for breast cancer patients.


Subject(s)
Breast Neoplasms/etiology , Disease Susceptibility , Fusobacterium Infections/complications , Fusobacterium nucleatum , Host-Pathogen Interactions , Animals , Autophagy/genetics , Autophagy/immunology , Biomarkers , Breast Neoplasms/metabolism , Breast Neoplasms/pathology , Female , Fusobacterium Infections/immunology , Fusobacterium Infections/microbiology , Fusobacterium nucleatum/immunology , Host Microbial Interactions , Host-Pathogen Interactions/immunology , Humans , Microbiota , Myeloid Differentiation Factor 88/genetics , Myeloid Differentiation Factor 88/metabolism , NF-kappa B/metabolism , Toll-Like Receptor 4/genetics , Toll-Like Receptor 4/metabolism
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