Serum amyloid A and inflammasome activation: A link to breast cancer progression?
| Autor: | Willem J.S. de Villiers, Anna-Mart Engelbrecht, Tanja Davis, Preetha Shridas, Carla Fourie |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Inflammasomes Endocrinology Diabetes and Metabolism Interleukin-1beta Immunology Breast Neoplasms Inflammation General Biochemistry Genetics and Molecular Biology Metastasis 03 medical and health sciences 0302 clinical medicine Breast cancer NLR Family Pyrin Domain-Containing 3 Protein Tumor Microenvironment Humans Immunology and Allergy Medicine Serum amyloid A Serum Amyloid A Protein Toll-like receptor business.industry Toll-Like Receptors Pattern recognition receptor Cancer Inflammasome medicine.disease 030104 developmental biology Cancer research medicine.symptom business 030215 immunology medicine.drug |
| Zdroj: | Cytokine & Growth Factor Reviews. 59:62-70 |
| ISSN: | 1359-6101 |
| DOI: | 10.1016/j.cytogfr.2020.10.006 |
| Popis: | Breast cancer is the most frequently diagnosed cancer in women globally. Although there have been many significant advances made in the diagnosis and treatment of breast cancer, numerous unresolved challenges remain, which include prevention, early diagnosis, metastasis and recurrence. The role of inflammation in cancer development is well established and is believed to be one of the leading hallmarks of cancer progression. Recently, the role of the inflammasome, a cytosolic multiprotein complex, has received attention in different cancers. By contributing to the activation of inflammatory cytokines the inflammasome intensifies the inflammatory cascade. The inflammasome can be activated through several pathways, which include the binding of pattern associated molecular patterns (PAMPs) and damage associated molecular patterns (DAMPs) to toll-like receptors (TLRs). Serum amyloid A (SAA), a non-specific acute-phase protein, can function as an endogenous DAMP by binding to pattern recognition receptors like TLRs on both breast cancer cells and cancer associated fibroblasts (CAFs). SAA can thus stimulate the production of IL-1β, thereby creating a favourable inflammatory environment to support tumour growth. The aim of this review is to highlight the possible role of SAA as an endogenous DAMP in the tumour microenvironment (TME) thereby promoting breast cancer growth through the activation of the NLRP3 inflammasome. |
| Databáze: | OpenAIRE |
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