Abstract
Abstract Introduction:Obesity and it's associated metabolic syndrome are known epidemiological risk factors for breast cancer.¹ Adipose tissue is a potent endocrine organ secreting many factors that can potentially regulate tumour growth. The breast constitutes an excellent model to determine the paracrine mediators of adiposity on breast cancer. The aim of this preliminary study was thus to describe the adipocytokine milieu in the breast and determine what influence adiposity and metabolic dysfunction played in tumour progression.Methods:Adipose conditioned media (ACM) was produced by harvesting adipose tissue from sites adjacent to (peritumoural PT) and distal (D) to tumour in 20 fresh mastectomy specimens and cultured in serum free media for 72hrs. MDA-MB 231 and MCF-7 cell lines were then cultured with this ACM for 24-48hrs. Cell survival/proliferation was determined by BrDU assay. An in depth characterisation of adipocytokine production from each adipose depot was performed using multiplex bead arrays.Results:ACM from peritumoural/distal adipose tissue promoted cell proliferation in both cell lines. The greatest proliferative effect was observed in ER+ve MCF-7 cell line relative to controls (151.9±7.3% and 150.8±9.8% in peritumoural and distal ACM respectively), compared to ER-ve MDA-MB-231 cells (111.4±5.0, 112.0±2.5%).PT ACM from metabolically unhealthy/obese patients significantly increased proliferation in MCF-7 cells, compared to normal weight cancer patients (171±12.6% vs 135.3±9.3%, p=0.034). Similarly, adipocytokine expression reflected these changes with expression differences in IL-6 (6.72±0.09, 6.31±0.16 ng/ml p=0.028), HGF (7.5±1.3, 3.98±0.43 ng/ml p=0.028).Conclusion:Peritumoural adipose tissue from metabolically unhealthy and obese patients increased cell proliferation compared to normal weight patients. Metabolic dysfunction influenced expression of several adipocytokines in ACM. A thorough analysis of this milieu should lead to a greater understanding of how obesity/metabolic dysfunction regulate tumourigenesis in breast cancer.
Published Version
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