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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Transient inhibition of synergistically insulin-like growth factor-1- and bisphenol A- induced poliferation of estrogen receptor alpha (ERalpha)-positive human breast cancer MCF-7 cells by melatonin.

There are many subclones of human breast cancer MCF-7 cells that respond to different levels of estrogen and that have been used for evaluating the estrogenic potential of environmental chemicals such as bisphenol A. In this study, I examined the effects of melatonin, an endogenous growth-inhibitory hormone, on the bisphenol A-induced proliferation of an MCF-7 subclone, designated as MCF-7-EMF cells. MCF-7-EMF cell growth was extremely slow in the presence of either estrogen at 10(-7) M or bisphenol A at 10(-7) M in a phenol-red-free medium and 10% charcoal-stripped fetal bovine serum. It was difficult to detect the increment of BrdU incorporation in MCF-7-EMF cells (2x10(4) cells) upon exposure to 10(-7) M bisphenol A alone for up to 50 h. The same result was obtained with cells exposed to 10 ng/ml insulin-like growth factor-1 (IGF-1) alone for up to 50 h. However, in the presence of 10 ng/ml IGF-1, bisphenol A markedly increased cell proliferation. The synergistic response was transiently inhibited by 10(-10) M melatonin (p<0.05). Thus, melatonin caused a transient inhibition of cell growth of estrogen receptor alpha (ERalpha)-positive MCF-7-EMF cells induced synergistically by both IGF-1 and bisphenol A.[1]


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