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
DC Field | Value | Language |
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dc.contributor.author | Kang, Nam-Hee | - |
dc.contributor.author | Hwang, Kyung-A. | - |
dc.contributor.author | Lee, Hye-Rim | - |
dc.contributor.author | Choi, Dal-Woong | - |
dc.contributor.author | Choi, Kyung-Chul | - |
dc.date.accessioned | 2021-09-05T22:11:39Z | - |
dc.date.available | 2021-09-05T22:11:39Z | - |
dc.date.created | 2021-06-14 | - |
dc.date.issued | 2013-09 | - |
dc.identifier.issn | 0278-6915 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/102299 | - |
dc.description.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. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | - |
dc.subject | EXPRESSING CYTOSINE-DEAMINASE | - |
dc.subject | INTERFERON-BETA MIGRATE | - |
dc.subject | BREAST-CANCER | - |
dc.subject | STEM-CELLS | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | INHIBITION | - |
dc.subject | ESTRADIOL | - |
dc.subject | APOPTOSIS | - |
dc.subject | TUMORS | - |
dc.title | 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 | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Choi, Dal-Woong | - |
dc.identifier.doi | 10.1016/j.fct.2013.06.029 | - |
dc.identifier.scopusid | 2-s2.0-84880376674 | - |
dc.identifier.wosid | 000324280000047 | - |
dc.identifier.bibliographicCitation | FOOD AND CHEMICAL TOXICOLOGY, v.59, pp.373 - 379 | - |
dc.relation.isPartOf | FOOD AND CHEMICAL TOXICOLOGY | - |
dc.citation.title | FOOD AND CHEMICAL TOXICOLOGY | - |
dc.citation.volume | 59 | - |
dc.citation.startPage | 373 | - |
dc.citation.endPage | 379 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Food Science & Technology | - |
dc.relation.journalResearchArea | Toxicology | - |
dc.relation.journalWebOfScienceCategory | Food Science & Technology | - |
dc.relation.journalWebOfScienceCategory | Toxicology | - |
dc.subject.keywordPlus | EXPRESSING CYTOSINE-DEAMINASE | - |
dc.subject.keywordPlus | INTERFERON-BETA MIGRATE | - |
dc.subject.keywordPlus | BREAST-CANCER | - |
dc.subject.keywordPlus | STEM-CELLS | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | ESTRADIOL | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | TUMORS | - |
dc.subject.keywordAuthor | Resveratrol | - |
dc.subject.keywordAuthor | IGF-1R | - |
dc.subject.keywordAuthor | ER alpha | - |
dc.subject.keywordAuthor | Cell proliferation | - |
dc.subject.keywordAuthor | Endocrine disrupting chemicals | - |
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