Abstract
Obesity is a significant risk factor for various cancers including breast cancer resulting in an increased risk of recurrence as well as morbidity and mortality. Extensive studies on various pathways have been successful in establishing a biological relationship between obesity and breast cancer. The molecular classification of breast cancer includes five groups each having different responses to treatment. Increased levels of inflammatory cytokines seen in obese conditions drive the pro-proliferative pathways, such as the influx of macrophages, angiogenesis, and antiapoptotic pathways. Increased peripheral aromatization of androgens by aromatase increases the circulating estrogen levels which are also responsible for the association of obesity with breast cancer. Also, increased oxidative stress due to chronic low-grade inflammation in obese women plays an important role in carcinogenesis. Despite the availability of safe and effective treatment options for breast cancer, obese women are at increased risk of adverse outcomes including treatment-related toxicities. In the recent decade, selenium compounds have gained substantial interest as chemopreventive and anticancer agents. The chemical derivatives of selenium include inorganic and organic compounds that exhibit pro-oxidant properties and alter cellular redox homeostasis. They target more than one metabolic pathway by thiol modifications, induction of reactive oxygen species, and chromatin modifications to exert their chemopreventive and anticancer activities. The primary functional effectors of selenium that play a significant role in human homeostasis are selenoproteins like glutathione peroxidase, thioredoxin reductase, iodothyronine deiodinases, and selenoprotein P. Selenoproteins play a significant role in adipose tissue physiology by modulating preadipocyte proliferation and adipogenic differentiation. They correlate negatively with body mass index resulting in increased oxidative stress that may lead to carcinogenesis in obese individuals. Methylseleninic acid effectively suppresses aromatase activation thus reducing the estrogen levels and acting as a breast cancer chemopreventive agent. Adipose-derived inflammatory mediators influence the selenium metabolites and affect the proliferation and metastatic properties of cancer cells. Recently selenium nanoparticles have shown potent anticancer activity which may lead to a major breakthrough in the management of cancers caused due to multiple pathways. In this review, we discuss the possible role of selenoproteins as chemopreventive and an anticancer agent in obese breast cancer.
Highlights
Obesity is a common disorder that leads to several health concerns like cardiovascular diseases, type 2 diabetes, and hypertension and increases the risk for many types of cancer such as breast, colorectal, esophagus, and pancreas
Selenoproteins are potent modifiers of carcinogenesis and tumor progression. They inhibit tumor development by revoking the oxidative stress insults in cancers that are driven by inflammatory mediators
Breast cancer and obesity both are chronic inflammatory conditions that present with increased oxidative stress and altered redox homeostasis
Summary
Obesity is a common disorder that leads to several health concerns like cardiovascular diseases, type 2 diabetes, and hypertension and increases the risk for many types of cancer such as breast, colorectal, esophagus, and pancreas. Studies have shown that approximately 20% of cancer cases are caused by excess weight and obesity which, in turn, may be due to a diet rich in fat and reduced physical activity (Wolin et al, 2010). Microarray-based gene expression profiling has revealed that breast cancers are intricate, and their histology is highly variable These studies have contributed their experimental results to classify tumors into different types based on the lymph node status, tumor grade, molecular type, and the presence of predictive markers such as estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor (HER2) (Perou et al, 1999; Holliday and Speirs, 2011). A prognostically important differentiation hierarchy occurs among all breast cancers and is classified into Luminal-A (ER+, PR+/−, HER2−), Luminal-B (ER+, PR+/−, HER2+), Basal/Triple-negative (ER−, PR−, HER2−), HER2 (ER−, PR−, HER2+) and Claudin-low (ER−, PR−, HER2−)
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