Abstract
Background: Obesity is considered as one of the risk factors for breast cancer. Leptin has been found to be involved in breast cancer progression. Therefore, novel approaches to antagonize biological effects of leptin are much needed. The objective of this study was to evaluate the protective effects of six dietary compounds (quercetin, curcumin, gallic acid, epigallocatechin gallate (EGCG), ascorbic acid and catechin) and assess the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in leptin-stimulated MCF-7 breast cancer cells in vitro. Methods: MCF-7 cells were exposed to leptin, leptin and compound and compound alone for 48 h. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide MTT and fluorometric assays after 48 h incubation. Phosphorylation of ERK1/2 was quantified by ELISA. Results: Only quercetin, curcumin and EGCG showed significant protective effects against leptin-induced proliferation of MCF-7 cells. Increase in ERK1/2 phosphorylation in response to leptin was reduced by the addition of quercetin, curcumin and EGCG. Conclusions: Considering the high prevalence of obesity, this observation provides a rationale for use of curcumin, quercetin and EGCG as antagonists of leptin in the treatment of obese breast cancer patients.
Highlights
Breast cancer is the most commonly diagnosed cancer among women in the world but there are limitations in patient care mostly due to inability of predicting outcome and limited treatment options [1]
All the compounds used in the study showed cytotoxic properties in MCF-7 breast cancer cells after a 48-h incubation period
Evidence from several in vitro studies shows a proliferative effect of leptin on cancer cells including MCF-7 breast cancer cells [6,7,8,9]
Summary
Breast cancer is the most commonly diagnosed cancer among women in the world but there are limitations in patient care mostly due to inability of predicting outcome and limited treatment options [1]. Several studies have indicated that levels of circulating metabolites such as adipokines, hormones, and cytokines are associated with breast cancer cell proliferation and migration [2,3]. Leptin is one such molecule considered to mediate breast cancer progression [4]. Leptin is a hormone mainly produced by white adipocytes It is synthesized by other organs/tissues including the mammary epithelium and placenta. Several studies have shown that leptin can exert proliferative effects on breast cancer cells in vitro [6,7,8,9]. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide MTT and fluorometric assays after
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