Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2012) 29 P755

ICEECE2012 Poster Presentations Endocrine Disruptors (26 abstracts)

Benzophenone-1 promoted cell growth of BG-1 ovarian cancer cells with estrogen receptors via progression of cell cycle

M. Park , H. Lee , E. Jeung & K. Choi


Chungbuk National University, Cheongju, Republic of Korea.


Benzophenones are organic chemicals widely used as stabilizers to UV light irradiation in plastic surface coatings and food packaging. They have been known that their derivatives appear to have cytotoxic effects. 2-Hydroxy-4-methoxybenzophenone (Benzophenone-3, BP-3) and its metabolite, 2,4-dihydroxybenzophenone (Benzophenone-1, BP-1), are used mostly in the formulation of nail polishes, enamels, bath products, sunscreens and skin care products. In this study, the estrogenic effects of BP-1 were examined in an ovarian cancer BG-1 cells expressing high levels of estrogen receptors (ERs) by an cell viability assay, semi-quantitative reverse-transcription PCR (semi-quantitative RT-PCR) and Western blot analysis. The treatment of BG-1 cells with BP-1 (10−8~10−5 M) resulted in an increase in their cell proliferation as 17-beta estradiol (E2) did. But, the cell growth stimulation by BP-1 was reversed by cotreatment with ICI 182,780, an ERs antagonist, suggesting that the proliferation of BG-1 cells is mediated by an ER-dependent pathway. In addition, BP-1 upregulated the expression levels of cell-cycle regulating genes, i.e., cyclin D1, which is a downstream target of ER, at 6 h after treatment. But, the expression of p21 gene was not altered by BP-1 at any time points. In translational levels, BP-1 also upregulated the expression level of cyclin D1 at 24 h after its treatment. Taken together, these results suggest that BP-1 is one of EDCs with have apparent estrogenic activities by stimulating cell proliferation of BG-1 cells and by inducing the expression of cyclin D1. Our results can support that BP-1 may have a potency to disrupt endocrine system and to stimulate cell growth in ER-positive cancer cells. [This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Ministry of Education, Science and Technology (MEST) of Korea government (no. 2011-0015385).]

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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