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The Influence of Endocrine Disrupting Chemicals on the Proliferation of ERα Knockdown-Human Breast Cancer Cell Line MCF-7; New Attempts by RNAi Technology
Bisphenol A (BPA) is a monomer use in manufacturing a wide range of chemical products which include epoxy resins and polycarbonate. It has been reported that BPA increases the cell proliferation activity of human breast cancer MCF-7 cells as well as 17-β estradiol (E2) and diethylstilbestrol (DES)....
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Formato: | Texto |
Lenguaje: | English |
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Japan Society of Histochemistry and Cytochemistry
2009
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685020/ https://www.ncbi.nlm.nih.gov/pubmed/19492024 http://dx.doi.org/10.1267/ahc.08036 |
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author | Miyakoshi, Takashi Miyajima, Katsuhiro Takekoshi, Susumu Osamura, Robert Yoshiyuki |
author_facet | Miyakoshi, Takashi Miyajima, Katsuhiro Takekoshi, Susumu Osamura, Robert Yoshiyuki |
author_sort | Miyakoshi, Takashi |
collection | PubMed |
description | Bisphenol A (BPA) is a monomer use in manufacturing a wide range of chemical products which include epoxy resins and polycarbonate. It has been reported that BPA increases the cell proliferation activity of human breast cancer MCF-7 cells as well as 17-β estradiol (E2) and diethylstilbestrol (DES). However, BPA induces target genes through ER-dependent and ER-independent manners which are different from the actions induced by E2. Therefore, BPA may be unique in estrogen-dependent cell proliferation compared to other endocrine disrupting chemicals (EDCs). In the present study, to test whether ERα is essential to the BPA-induced proliferation on MCF-7 cells, we suppressed the ERα expression of MCF-7 cells by RNA interference (RNAi). Proliferation effects in the presence of E2, DES and BPA were not observed in ERα-knockdown MCF-7 cells in comparison with control MCF-7. In addition, a marker of proliferative potential, MIB-1 labeling index (LI), showed no change in BPA-treated groups compared with vehicle-treated groups on ERα-knockdown MCF-7 cells. In conclusion, we demonstrated that ERα has a role in BPA-induced cell proliferation as well as E2 and DES. Moreover, this study indicated that the direct knockdown of ERα using RNAi serves as an additional tool to evaluate, in parallel with MCF-7 cell proliferation assay, for potential EDCs. |
format | Text |
id | pubmed-2685020 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Japan Society of Histochemistry and Cytochemistry |
record_format | MEDLINE/PubMed |
spelling | pubmed-26850202009-06-02 The Influence of Endocrine Disrupting Chemicals on the Proliferation of ERα Knockdown-Human Breast Cancer Cell Line MCF-7; New Attempts by RNAi Technology Miyakoshi, Takashi Miyajima, Katsuhiro Takekoshi, Susumu Osamura, Robert Yoshiyuki Acta Histochem Cytochem Regular Article Bisphenol A (BPA) is a monomer use in manufacturing a wide range of chemical products which include epoxy resins and polycarbonate. It has been reported that BPA increases the cell proliferation activity of human breast cancer MCF-7 cells as well as 17-β estradiol (E2) and diethylstilbestrol (DES). However, BPA induces target genes through ER-dependent and ER-independent manners which are different from the actions induced by E2. Therefore, BPA may be unique in estrogen-dependent cell proliferation compared to other endocrine disrupting chemicals (EDCs). In the present study, to test whether ERα is essential to the BPA-induced proliferation on MCF-7 cells, we suppressed the ERα expression of MCF-7 cells by RNA interference (RNAi). Proliferation effects in the presence of E2, DES and BPA were not observed in ERα-knockdown MCF-7 cells in comparison with control MCF-7. In addition, a marker of proliferative potential, MIB-1 labeling index (LI), showed no change in BPA-treated groups compared with vehicle-treated groups on ERα-knockdown MCF-7 cells. In conclusion, we demonstrated that ERα has a role in BPA-induced cell proliferation as well as E2 and DES. Moreover, this study indicated that the direct knockdown of ERα using RNAi serves as an additional tool to evaluate, in parallel with MCF-7 cell proliferation assay, for potential EDCs. Japan Society of Histochemistry and Cytochemistry 2009-04-28 2009-04-03 /pmc/articles/PMC2685020/ /pubmed/19492024 http://dx.doi.org/10.1267/ahc.08036 Text en © 2009 The Japan Society of Histochemistry and Cytochemistry This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Regular Article Miyakoshi, Takashi Miyajima, Katsuhiro Takekoshi, Susumu Osamura, Robert Yoshiyuki The Influence of Endocrine Disrupting Chemicals on the Proliferation of ERα Knockdown-Human Breast Cancer Cell Line MCF-7; New Attempts by RNAi Technology |
title | The Influence of Endocrine Disrupting Chemicals on the Proliferation of ERα Knockdown-Human Breast Cancer Cell Line MCF-7; New Attempts by RNAi Technology |
title_full | The Influence of Endocrine Disrupting Chemicals on the Proliferation of ERα Knockdown-Human Breast Cancer Cell Line MCF-7; New Attempts by RNAi Technology |
title_fullStr | The Influence of Endocrine Disrupting Chemicals on the Proliferation of ERα Knockdown-Human Breast Cancer Cell Line MCF-7; New Attempts by RNAi Technology |
title_full_unstemmed | The Influence of Endocrine Disrupting Chemicals on the Proliferation of ERα Knockdown-Human Breast Cancer Cell Line MCF-7; New Attempts by RNAi Technology |
title_short | The Influence of Endocrine Disrupting Chemicals on the Proliferation of ERα Knockdown-Human Breast Cancer Cell Line MCF-7; New Attempts by RNAi Technology |
title_sort | influence of endocrine disrupting chemicals on the proliferation of erα knockdown-human breast cancer cell line mcf-7; new attempts by rnai technology |
topic | Regular Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685020/ https://www.ncbi.nlm.nih.gov/pubmed/19492024 http://dx.doi.org/10.1267/ahc.08036 |
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