Document Detail


Induced growth of BG-1 ovarian cancer cells by 17β-estradiol or various endocrine disrupting chemicals was reversed by resveratrol via downregulation of cell cycle progression.
MedLine Citation:
PMID:  22552626     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Resveratrol (trans-3,4',5-trihydroxystilbene; RES), a phytoestrogen, exists in grape skin and red wine. Endocrine disrupting chemicals (EDCs) appear to promote the development and progression of estrogen-dependent cancers. In this study, we evaluated the inhibitory effect of RES on the cell proliferation induced by various EDCs in BG-1 ovarian cancer cells. Various EDCs, such as bisphenol A (BPA), nonylphenol (NP), octylphenol (OP), methoxychlor (MXC) and hexabromocyclododecane (HBCD), were employed in this study. In the in vitro experiments, treatment of BG-1 cells with E2, BPA, NP, OP, MXC or HBCD resulted in an increase of cell growth. By contrast, increased cell viability induced by these EDCs was reversed when co-cultured with RES. In addition, we examined the regulation of cell cycle-related genes by RT-PCR and western blot analysis. Treatment with each EDC was found to decrease only the gene expression of p21 and increase the expression of cell cycle-dependent kinase 2 (CDK2). However, co-treatment with RES and each EDC resulted in an increased gene expression of p21 and a decreased expression of CDK2. Cyclin D1 was increased by downregulating p21 only when treated with each EDC in the absence of RES, while co-treatment with RES and each EDC decreased the gene expression of cyclin D1 by upregulating p21. Taken together, RES appears to be an inhibitor of cyclin D1 and CDK2 and is responsible for the cell cycle arrest at the G1 phase. In addition, when co-treated with each EDC, RES increased the expression of p21 and resulted in the growth inhibition of BG-1 ovarian cancer cells. Taken together, these results indicate the antiproliferative effect of RES, a dietary phytoestrogen, on estrogen-dependent ovarian cancer cells activated by EDCs.
Authors:
Nam-Hee Kang; Kyung-A Hwang; Tae-Hee Kim; Sang-Hwan Hyun; Eui-Bae Jeung; Kyung-Chul Choi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-04-23
Journal Detail:
Title:  Molecular medicine reports     Volume:  6     ISSN:  1791-3004     ISO Abbreviation:  Mol Med Rep     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-05-09     Completed Date:  2012-09-10     Revised Date:  2013-06-03    
Medline Journal Info:
Nlm Unique ID:  101475259     Medline TA:  Mol Med Rep     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  151-6     Citation Subset:  IM    
Affiliation:
College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea.
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MeSH Terms
Descriptor/Qualifier:
Antineoplastic Agents, Phytogenic / pharmacology*
Cell Cycle / drug effects*,  genetics
Cell Cycle Proteins / genetics,  metabolism
Cell Line, Tumor
Cell Proliferation / drug effects
Down-Regulation / drug effects
Endocrine Disruptors / pharmacology*
Estradiol / pharmacology*
Female
Humans
Ovarian Neoplasms / genetics*,  metabolism*
Stilbenes / pharmacology*
Chemical
Reg. No./Substance:
0/Antineoplastic Agents, Phytogenic; 0/Cell Cycle Proteins; 0/Endocrine Disruptors; 0/Stilbenes; 50-28-2/Estradiol; Q369O8926L/resveratrol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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