TNF-Alpha Promotes an Inflammatory Mammary Microenvironment That Favors Macrophage and Epithelial Migration in a CCL2- and Mitochondrial-ROS-Dependent Manner.
María Jesús VeraFrancisco GuajardoFelix A UrraNicolás TobarJorge MartínezPublished in: Antioxidants (Basel, Switzerland) (2023)
The influence of an inflammatory microenvironment on tumorigenesis has been widely accepted. Systemic conditions that favor the onset of an inflammatory landscape predispose the progression of breast cancer. Under obesity conditions, the endocrine function of adipose tissue is one of the main determinants of the production of local and systemic inflammatory mediators. Although these mediators can stimulate tumorigenesis and recruit inflammatory cells, as macrophages, the mechanism involved remains poorly understood. In the present work, we describe that the TNFα treatment of mammary preadipocytes from human normal patients blocks adipose differentiation and promotes the generation of pro-inflammatory soluble factors. The latter stimulate the mobilization of THP-1 monocytes and MCF-7 epithelial cancer cells in an MCP1/CCL2- and mitochondrial-ROS-dependent manner. Together, these results reaffirm the contribution of an inflammatory microenvironment and mtROS in the progression of breast cancer.
Keyphrases
- oxidative stress
- adipose tissue
- stem cells
- insulin resistance
- rheumatoid arthritis
- endothelial cells
- induced apoptosis
- cell death
- end stage renal disease
- chronic kidney disease
- dna damage
- physical activity
- newly diagnosed
- weight loss
- cell proliferation
- ejection fraction
- immune response
- body mass index
- high fat diet
- liver injury
- peritoneal dialysis
- high fat diet induced
- drug induced
- young adults