scholarly journals Gene Alterations of Ovarian Cancer Cells Expressing Estrogen Receptors by Estrogen and Bisphenol A Using Microarray Analysis

2011 ◽  
Vol 27 (2) ◽  
pp. 99 ◽  
Author(s):  
Kyung-A Hwang ◽  
Se-Hyung Park ◽  
Bo-Rim Yi ◽  
Kyung-Chul Choi
Keyword(s):  
Ovarian Cancer ◽  
Bisphenol A ◽  
Estrogen Receptors ◽  
Cancer Cells ◽  
Microarray Analysis ◽  
Ovarian Cancer Cells ◽  
Gene Alterations

152 BISPHENOL A AND 17-BETA-OESTRADIOL RESULTED IN THE GENE ALTERATIONS IN OESTROGEN-RECEPTOR POSITIVE BG-1 OVARIAN CANCER CELLS

2012 ◽  
Vol 24 (1) ◽  
pp. 188
Author(s):  
K.-A Hwang ◽  
S.-H. Hyun ◽  
E.-B. Jeung ◽  
K.-C. Choi
Keyword(s):  
Ovarian Cancer ◽  
Bisphenol A ◽  
Cancer Cells ◽  
Oestrogen Receptor ◽  
Endocrine Disrupting Chemicals ◽  
Ovarian Cancer Cells ◽  
Mrna Levels ◽  
Endocrine Disrupting ◽  
Er Positive ◽  
Gene Alterations

Because endocrine disrupting chemicals may interfere with the endocrine systems of our body and have an oestrogenic activity, we evaluated the effects of bisphenol A (BPA) on the transcriptional levels of altered genes in oestrogen receptor (ER)-positive BG-1 ovarian cancer cells. A microarray and RT-qPCR were employed to detect gene alterations in these cells following treatments. In this study, treatment with 17-β-oestradiol (E2) or BPA increased mRNA levels of E2-responsive genes related to apoptosis, cancer and cell cycle, signal transduction and nucleic acid binding and so on. Parallel with the microarray data, the mRNA levels of some altered genes including RAB31_member RAS oncogene family (U59877), cyclin D1 (X59798), cyclin-dependent kinase 4 (U37022), IGF-binding protein 4 (U20982) and anti-mullerian hormone (NM_000479) were significantly induced by E2 or BPA in this cell model. These results indicate that BPA in parallel with E2 induced the transcriptional levels of E2-responsive genes in an ER-positive BG-1 cells. In conclusion, these microarray and RT-qPCR results indicate that BPA, a potential weak oestrogen, may have an oestrogenic effect by regulating E2-responsive genes in ER-positive BG-1 cells and that BG-1 cells would be the best in vitro model to detect these oestrogenic endocrine disrupting chemicals. This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 2011-0015385).

192 RESVERATROL, A NATURAL FOOD COMPOUND, SUPPRESSED THE CELL GROWTH OF BG-1 OVARIAN CANCER CELLS INDUCED BY 17β-ESTRADIOL OR BISPHENOL A THROUGH DOWNREGULATING ESTROGEN RECEPTOR α AND INSULIN-LIKE GROWTH FACTOR-1 RECEPTOR

2013 ◽  
Vol 25 (1) ◽  
pp. 245
Author(s):  
N.-H. Kang ◽  
K.-C. Choi
Keyword(s):  
Ovarian Cancer ◽  
Growth Factor ◽  
Cell Growth ◽  
Bisphenol A ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Insulin Like Growth Factor ◽  
Cancer Cell Growth

Resveratrol (trans-3,4,5-trihydroxystilbene; RES) was adopted in this study as a novel phytoestrogen displaying antioxidant, antiinflammatory, and anticancer effects. In this study, we evaluated the inhibitory effect of RES on the cell growth induced by 17β-oestradiol (E2), a typical oestrogen, and bisphenol A (BPA), an endocrine-disrupting chemical (EDC) in BG-1 ovarian cancer cells expressing oestrogen receptors (ER) through down-regulating oestrogen receptor α (ERa) and insulin-like growth factor-1 receptor (IGF-1R). The EDC and oestrogen appear to promote the development of the oestrogen-dependent cancers. Thus, we need to develop therapeutic methods for EDC-dependent cancers. In in vitro experiments, we examined the cell viability and mRNA expression of ERa ± IGF-1R genes following the treatments with E2 or BPA in the presence or absence of RES or ICI 182 780, an ER antagonist, by MTT assay and RT-PCR, respectively. We also examined the protein level of ERa, phosphorylated insulin receptor substrate-1 (IRS-1), phosphorylated Akt1/2/3, p21, and cyclin D1 by Western blot analysis. Treatment with E2 or BPA remarkably increased the growth of BG-1 ovarian cancer cells, and their enhanced cell growth appeared to be mediated by ERa. In addition, the treatment of BG-1 ovarian cancer cells with E2 or BPA resulted in an increase in ERa and IGF-1R gene expressions. However, co-treatment of RES reversed E2- or BPA-induced ovarian cancer cell growth and mRNA expressions of ERa and IGF-1R. The protein levels of phosphorylated IRS-1 and Akt were upregulated by E2 or BPA, whereas these levels were downregulated by co-treatment of RES in the presence of E2 or BPA. Taken together, these results indicate that RES may effectively inhibit ovarian cancer cell growth via downregulating cross-talk between ERa and IGF-1R. 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).

191 RISK ASSESSMENT OF BISPHENOL A, AN ENDOCRINE DISRUPTOR, VIA PROLIFERATIVE EFFECT ON THE GROWTH OF ESTROGEN-DEPENDENT OVARIAN CANCER IN CELLULAR AND ANIMAL MODELS

2013 ◽  
Vol 25 (1) ◽  
pp. 244
Author(s):  
K.-A. Hwang ◽  
K.-C. Choi
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Bisphenol A ◽  
Cancer Cells ◽  
The Body ◽  
Brdu Incorporation ◽  
Ovarian Cancer Cells ◽  
Tumour Proliferation

One of estrogens in the body, 17β-oestradiol (E2), is a pleiotropic hormone that regulates the growth and differentiation of many tissues and also acts as a mitogen that promotes the development and proliferation of hormone-responsive cancers such as breast and ovarian carcinomas. Xenoestrogens are chemical compounds that imitate oestrogen in living organisms and are classified as a type of endocrine-disrupting chemical (EDC). Bisphenol A (BPA) is a widely used industrial compound, and also known as an EDC and especially a xenoestrogen. In this study, we examined the effect of E2 or BPA on the cell growth of BG-1 ovarian cancer cells in vivo and in vitro. In the cell proliferation assay in vitro, E2 or BPA increased the growth of the BG-1 ovarian cancer cells expressing oestrogen receptors (ER). Their proliferation activity was reversed by the treatment of ICI 182 780, a well-known antagonist of ER, which demonstrates that the cell proliferation by E2 or BPA is mediated by ER and BPA certainly acts as a xenoestrogen in the BG-1 ovarian cancer cells. Clearly, E2 and BPA increased the expression of cyclin D1, a factor responsible for the G1/S cell cycle transition. These reagents also decreased the expression of p21, a potent cyclin-dependent kinase (CDK) inhibitor that arrests the cell cycle in the G1 phase. As a result, they promoted the proliferation of BG-1 cells via upregulation of the cell cycle progression. In mice xenograft models transplanted with BG-1 ovarian cancer cells, E2 or BPA administration significantly induced the tumour proliferation compared with vehicle (corn oil) treatment for 10 weeks, which was identified by the measurement of tumour volume and histological analysis on tumour tissues such as hematoxylin and eosin (H&E) staining and BrdU incorporation assay. Taken together, as an EDC having a xenoestrogenic activity, BPA was demonstrated to have a risk of tumour proliferation in oestrogen-dependent cancers such as ovarian cancer. This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Ministry of Education, Science and Technology (MEST) of government of Korea (no. 2011-0015385).

204 ALTERED GENE EXPRESSION FOLLOWING EXPOSURE TO BISPHENOL A IN HUMAN OVARIAN CANCER CELLS EXPRESSING ESTROGEN RECEPTORS BY MICROARRAY

2011 ◽  
Vol 23 (1) ◽  
pp. 201 ◽  
Author(s):  
B.-R. Yi ◽  
E.-B. Jeung ◽  
K.-C. Choi
Keyword(s):  
Gene Expression ◽  
Ovarian Cancer ◽  
Growth Factor ◽  
Bisphenol A ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Altered Gene Expression ◽  
Ovarian Cells ◽  
Altered Gene

Although endocrine-disrupting chemicals (EDC) may interfere with the endocrine system(s) of animals and humans and have an estrogenicity or androgenicity, the exact mechanism(s) underlying their detrimental effects is not clearly understood. Among them, bisphenol A (BPA) is widespread in the environment and is commonly ingested by animals because it is used in the manufacture of polycarbonate plastics, food-storage containers, and other plastics. Thus, in this study, we evaluated altered gene expression following exposure to BPA by microarry in human ovarian cancer cells, which highly express oestrogen receptors (ER). Treatment with BPA and endogenous oestrogen (E2) for 24 h resulted in an increase in cell proliferation and enhanced the oestrogen response element (ERE) activity in human BG-1 ovarian cancer cells with ER. Bisphenol A-induced cell growth and the activation of ERE were reversed by an oestrogen receptor antagonist, ICI 182 780, suggesting that ER appear to be involved in BPA-induced cell growth and ERE activation in these ovarian cells. Following BPA treatment, the expression levels of representative genes, namely, apoptosis inhibitor 4 (survivin), RAB31 ras oncogene family, v-myc, v-myb, cyclin A2, cyclin B1, amphiregulin, insulin-like growth factor binding protein 4, chemokine-like factor 3, fibroblast growth factor, and E2F transcription factor 4, were subsequently confirmed in these ovarian cells by real-time PCR. Taken together, these results indicate distinctly altered expression of responsive genes following exposure to BPA, and implicate distinct effects of endogenous E2 and environmental EDC in human ovarian cancer cells expressing ER. This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST; No. 2010-0003093).

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