Abstract
Background TCEP is an organophosphorus flame-retardant (OPFR) widely used in polyurethane foams and household products. From these materials, TCEP emits into the surrounding environment, which humans encounter through inhalation and dermal absorption. Previous studies have shown OPFRs to have endocrine disrupting actions, and thus, influence diseases such as cancer. Breast cancer is the second most common cancer among women in the United States, and because of this prevalence, it is imperative to investigate possible carcinogens. Due to the endocrine disrupting nature of OPFRs, we are investigating the effects of TCEP on hormone-dependent breast cancer cell lines MCF-7 and T-47D. Methods Our study examines the effects of TCEP, alone and in combination with hormones and anti- hormones, on ERα and BRCA-1 expression in MCF-7 and T-47D breast cancer cell lines by utilizing western blot analyses, cellular viability assays, confocal microscopy, and RT-qPCR analyses. In order to deplete any endogenous steroids or effectors, breast cancer cells were cultured in a medium containing 5% charcoal-stripped fetal bovine serum for six days. Results Western blot analysis revealed alterations in ERα and BRCA-1 expression after 24 hours of treatment with varying TCEP concentrations (1μM-2mM). Analysis revealed a concentration- dependent increase in BRCA-1 expression in both cell lines, and a concentration-dependent decrease in ERα expression in the T-47D cell line. During hormonal studies, cells were treated with an optimum concentration of TCEP along with combinations of hormones and anti- hormones. After 24-hour treatment with a combination of E2 + TCEP, a significant decrease in ERα expression was observed in both cell lines. A significant increase of BRCA-1 expression occurred after 24-hour treatment of TCEP + E2 in both cell lines. These effects were sensitive to the presence of antiestrogens. Cellular viability assays revealed a significant increase in cellular viability in both cell lines when treated with a combination of E2 + TCEP. Conclusion Our results suggest that TECP acts as an endocrine disrupting compound on the steroid receptors and tumor suppressor genes in breast cancer cells. Further studies are warranted to determine the exact mechanism of action and influence of TCEP on breast cancer progression.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call