Resveratrol regulates the cell viability promoted by 17 beta-estradiol or bisphenol A via down-regulation of the cross-talk between estrogen receptor alpha and insulin growth factor-1 receptor in BG-1 ovarian cancer cells
- Authors
- Kang, Nam-Hee; Hwang, Kyung-A.; Lee, Hye-Rim; Choi, Dal-Woong; Choi, Kyung-Chul
- Issue Date
- 9월-2013
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- Resveratrol; IGF-1R; ER alpha; Cell proliferation; Endocrine disrupting chemicals
- Citation
- FOOD AND CHEMICAL TOXICOLOGY, v.59, pp.373 - 379
- Indexed
- SCIE
SCOPUS
- Journal Title
- FOOD AND CHEMICAL TOXICOLOGY
- Volume
- 59
- Start Page
- 373
- End Page
- 379
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/102299
- DOI
- 10.1016/j.fct.2013.06.029
- ISSN
- 0278-6915
- Abstract
- Endocrine disrupting chemicals (EDCs) and estrogens appear to promote development of estrogen-dependent cancers, including breast and ovarian carcinomas. In this study, we evaluated the cell viability effect of BPA on BG-1 human ovarian cancer cells, along with the growth inhibitory effect of resveratrol (trans-3,4,5-trihydroxystilbene; RES), a naturally occurring phytoestrogen. In addition, we investigated the underlying mechanism(s) of BPA and RES in regulating the interaction between estrogen receptor alpha (ER alpha) and insulin-like growth factor-1 receptor (IGF-1R) signals, a non- genomic pathway induced by 17 beta-estradiol (E2). BPA induced a significant increase in BG-1 cell growth and up-regulated mRNA levels of ER alpha and IGF-1R. In parallel with its mRNA level, the protein expression of ER alpha was induced, and phosphorylated insulin receptor substrate-1 (p-IRS-1), phosphorylated Akt1/2/3, and cyclin D1 were increased by BPA or E2. However, RES effectively reversed the BG-1 cell proliferation induced by E2 or BPA by inversely down-regulating the expressions of ER alpha, IGF-1R, p-IRS-1, and p-Akt1/2/3, and cyclin D1 at both transcriptional and translational levels. Taken together, these results suggest that RES is a novel candidate for prevention of tumor progression caused by EDCs, including BPA via effective inhibition of the cross-talk of ER alpha and IGF-1R signaling pathways. (c) 2013 Elsevier Ltd. All rights reserved.
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