Obesity, a physiological situation where different proinflammatory cytokines and hormones are secreted, is a major risk factor for breast cancer. Mitochondrial functionality exhibits a relevant role in the tumorigenic potential of a cancer cell. In the present study, it has been examined the influence of an obesity-related inflammation ELIT treatment (17β-estradiol, leptin, IL-6, and TNFα), which aims to stimulate the hormonal conditions of a postmenopausal obese woman on the mitochondrial functionality and invasiveness of MCF7 and T47D breast cancer cell lines, which display a different ratio of both estrogen receptor isoforms, ERα and ERβ. The results showed a decrease in mitochondrial functionality, with an increase in oxidative stress and invasiveness and motility, in the MCF7 cell line (high ERα/ERβ ratio) compared to a maintained status in the T47D cell line (low ERα/ERβ ratio) after ELIT treatment. In addition, breast cancer biopsies were analyzed, showing that breast tumors of obese patients present a high positive correlation between IL-6 receptor and ERβ and have an increased expression of cytokines, antioxidant enzymes, and mitochondrial biogenesis and dynamics genes. Altogether, giving special importance to ERβ in the pathology of obese patients with breast cancer is necessary, approaching to personalized medicine.
Keywords: breast cancer; epithelial-to-mesenchymal transition (EMT); estrogen receptor beta (ERβ); mitochondrial biogenesis; mitochondrial dynamics; obesity-related inflammation; oxidative stress.