17β‐estradiol upregulates GREB1 and accelerates ovarian tumor progression in vivo
Exogenous 17β‐estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG‐LS‐TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian t...
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| Veröffentlicht in: | International journal of cancer Jg. 135; H. 5; S. 1072 - 1084 |
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Wiley-Blackwell
01.09.2014
BlackWell Publishing Ltd |
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| Abstract | Exogenous 17β‐estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG‐LS‐TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumor progression. Mouse ovarian cancer ascites (MAS) cell lines were derived from tgCAG‐LS‐TAg mice. Following intraperitoneal engraftment of two MAS cell lines, MASC1 and MASE2, into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumor burden. Microarray analysis performed on MASE2‐derived tumors treated with E2 or placebo showed that E2 treatment caused the upregulation of 197 genes and the downregulation of 55 genes. The expression of gene regulated by estrogen in breast cancer 1 (Greb1) was upregulated in mouse tumors treated with E2 and was overexpressed in human ovarian cancers relative to human ovarian surface epithelium, suggesting a role for GREB1 in human ovarian tumor progression. RNA interference‐mediated knockdown of GREB1 in MASE2 cells decreased their proliferation rate in vitro and increased survival time in mice engrafted with the cells. These results emphasize the importance of E2 in ovarian tumor progression and identify Greb1 as a novel gene target for therapeutic intervention.
What's new?
Post‐menopausal estrogen‐only hormone replacement therapy is associated with an increased risk of epithelial ovarian cancer, the development of which may be influenced by the actions of 17β‐estradiol (E2) on ovarian surface epithelium (OSE). Here, in an orthotopic mouse model of ovarian cancer, E2 was found to accelerate tumor progression. Microarray analysis identified 197 E2‐upregulated and 55 E2‐downregulated genes. Among E2‐upregulated genes was Greb1. GREB1 protein was highly upregulated in human tumors relative to normal human OSE, suggesting that it may be a tumor‐promoting factor and potential mediator of E2‐stimulated tumor growth. |
|---|---|
| AbstractList | Exogenous 17β‐estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG‐LS‐TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumor progression. Mouse ovarian cancer ascites (MAS) cell lines were derived from tgCAG‐LS‐TAg mice. Following intraperitoneal engraftment of two MAS cell lines, MASC1 and MASE2, into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumor burden. Microarray analysis performed on MASE2‐derived tumors treated with E2 or placebo showed that E2 treatment caused the upregulation of 197 genes and the downregulation of 55 genes. The expression of gene regulated by estrogen in breast cancer 1 (
Greb1
) was upregulated in mouse tumors treated with E2 and was overexpressed in human ovarian cancers relative to human ovarian surface epithelium, suggesting a role for GREB1 in human ovarian tumor progression. RNA interference‐mediated knockdown of GREB1 in MASE2 cells decreased their proliferation rate
in vitro
and increased survival time in mice engrafted with the cells. These results emphasize the importance of E2 in ovarian tumor progression and identify
Greb1
as a novel gene target for therapeutic intervention.
What's new?
Post‐menopausal estrogen‐only hormone replacement therapy is associated with an increased risk of epithelial ovarian cancer, the development of which may be influenced by the actions of 17β‐estradiol (E2) on ovarian surface epithelium (OSE). Here, in an orthotopic mouse model of ovarian cancer, E2 was found to accelerate tumor progression. Microarray analysis identified 197 E2‐upregulated and 55 E2‐downregulated genes. Among E2‐upregulated genes was
Greb1
. GREB1 protein was highly upregulated in human tumors relative to normal human OSE, suggesting that it may be a tumor‐promoting factor and potential mediator of E2‐stimulated tumor growth. Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumor progression. Mouse ovarian cancer ascites (MAS) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of two MAS cell lines, MASC1 and MASE2, into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumor burden. Microarray analysis performed on MASE2-derived tumors treated with E2 or placebo showed that E2 treatment caused the upregulation of 197 genes and the downregulation of 55 genes. The expression of gene regulated by estrogen in breast cancer 1 (Greb1) was upregulated in mouse tumors treated with E2 and was overexpressed in human ovarian cancers relative to human ovarian surface epithelium, suggesting a role for GREB1 in human ovarian tumor progression. RNA interference-mediated knockdown of GREB1 in MASE2 cells decreased their proliferation rate in vitro and increased survival time in mice engrafted with the cells. These results emphasize the importance of E2 in ovarian tumor progression and identify Greb1 as a novel gene target for therapeutic intervention. Exogenous 17β‐estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG‐LS‐TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumor progression. Mouse ovarian cancer ascites (MAS) cell lines were derived from tgCAG‐LS‐TAg mice. Following intraperitoneal engraftment of two MAS cell lines, MASC1 and MASE2, into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumor burden. Microarray analysis performed on MASE2‐derived tumors treated with E2 or placebo showed that E2 treatment caused the upregulation of 197 genes and the downregulation of 55 genes. The expression of gene regulated by estrogen in breast cancer 1 (Greb1) was upregulated in mouse tumors treated with E2 and was overexpressed in human ovarian cancers relative to human ovarian surface epithelium, suggesting a role for GREB1 in human ovarian tumor progression. RNA interference‐mediated knockdown of GREB1 in MASE2 cells decreased their proliferation rate in vitro and increased survival time in mice engrafted with the cells. These results emphasize the importance of E2 in ovarian tumor progression and identify Greb1 as a novel gene target for therapeutic intervention. What's new? Post‐menopausal estrogen‐only hormone replacement therapy is associated with an increased risk of epithelial ovarian cancer, the development of which may be influenced by the actions of 17β‐estradiol (E2) on ovarian surface epithelium (OSE). Here, in an orthotopic mouse model of ovarian cancer, E2 was found to accelerate tumor progression. Microarray analysis identified 197 E2‐upregulated and 55 E2‐downregulated genes. Among E2‐upregulated genes was Greb1. GREB1 protein was highly upregulated in human tumors relative to normal human OSE, suggesting that it may be a tumor‐promoting factor and potential mediator of E2‐stimulated tumor growth. Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumor progression. Mouse ovarian cancer ascites (MAS) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of two MAS cell lines, MASC1 and MASE2, into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumor burden. Microarray analysis performed on MASE2-derived tumors treated with E2 or placebo showed that E2 treatment caused the upregulation of 197 genes and the downregulation of 55 genes. The expression of gene regulated by estrogen in breast cancer 1 (Greb1) was upregulated in mouse tumors treated with E2 and was overexpressed in human ovarian cancers relative to human ovarian surface epithelium, suggesting a role for GREB1 in human ovarian tumor progression. RNA interference-mediated knockdown of GREB1 in MASE2 cells decreased their proliferation rate in vitro and increased survival time in mice engrafted with the cells. These results emphasize the importance of E2 in ovarian tumor progression and identify Greb1 as a novel gene target for therapeutic intervention.Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumor progression. Mouse ovarian cancer ascites (MAS) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of two MAS cell lines, MASC1 and MASE2, into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumor burden. Microarray analysis performed on MASE2-derived tumors treated with E2 or placebo showed that E2 treatment caused the upregulation of 197 genes and the downregulation of 55 genes. The expression of gene regulated by estrogen in breast cancer 1 (Greb1) was upregulated in mouse tumors treated with E2 and was overexpressed in human ovarian cancers relative to human ovarian surface epithelium, suggesting a role for GREB1 in human ovarian tumor progression. RNA interference-mediated knockdown of GREB1 in MASE2 cells decreased their proliferation rate in vitro and increased survival time in mice engrafted with the cells. These results emphasize the importance of E2 in ovarian tumor progression and identify Greb1 as a novel gene target for therapeutic intervention. |
| Author | Perez‐Iratxeta, Carol Hodgkinson, Kendra M. Laviolette, Laura A. Vanderhyden, Barbara C. Minhas, Neha |
| Author_xml | – sequence: 1 givenname: Laura A. surname: Laviolette fullname: Laviolette, Laura A. organization: Centre for Cancer Therapeutics, Ottawa Hospital Research Institute – sequence: 2 givenname: Kendra M. surname: Hodgkinson fullname: Hodgkinson, Kendra M. organization: Centre for Cancer Therapeutics, Ottawa Hospital Research Institute – sequence: 3 givenname: Neha surname: Minhas fullname: Minhas, Neha organization: Centre for Cancer Therapeutics, Ottawa Hospital Research Institute – sequence: 4 givenname: Carol surname: Perez‐Iratxeta fullname: Perez‐Iratxeta, Carol organization: Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute – sequence: 5 givenname: Barbara C. surname: Vanderhyden fullname: Vanderhyden, Barbara C. organization: University of Ottawa |
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| Keywords | Animal model mouse model ovarian cancer Ovary cancer Rodentia Estrogen GREB1 17β-Estradiol Malignant tumor Ovarian hormone Female genital diseases Ovarian diseases In vivo Vertebrata microarray Mammalia Cancerology Mouse Tumor progression Sex steroid hormone Cancer Ovarian tumor estrogen |
| Language | English |
| License | Attribution-NonCommercial-NoDerivs http://creativecommons.org/licenses/by-nc-nd/3.0 CC BY 4.0 2014 The Authors. Published by Wiley Periodicals, Inc. on behalf of UICC. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
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| Notes | L.A.L and K.M.H. contributed equally to this work ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Grant sponsor: Ovarian Cancer Canada for its financial support of the Ottawa Ovarian Cancer Tissue Bank, Canadian Institutes of Health Research (B.C.V.), a doctoral research award from the Canadian Institutes of Health Research-Ontario Women’s Health Council/Institute of Gender and Health (L.A.L.), a Frederick Banting and Charles Best Canada Graduate Scholarship Master’s Award (K.M.H.), an Ontario Graduate Scholarship (K.M.H.), a doctoral research award from the CIHR Training Program in Reproduction, Early Development and the Impact on Health (K.M.H.), Teal Heart award from Ovarian Cancer Canada (K.M.H.) |
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| Snippet | Exogenous 17β‐estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG‐LS‐TAg mouse model of the disease. We hypothesized that E2... Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2... |
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| SubjectTerms | Animals Biological and medical sciences Cancer Genetics Carcinoma, Ovarian Epithelial Cell Line, Tumor Cell Proliferation Disease Progression Down-Regulation Estradiol - pharmacology estrogen Female Female genital diseases Gene Expression Regulation, Neoplastic - drug effects GREB1 Gynecology. Andrology. Obstetrics Humans Medical sciences Mice Mice, SCID microarray mouse model Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Neoplasms, Glandular and Epithelial - genetics Neoplasms, Glandular and Epithelial - pathology ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology RNA Interference RNA, Small Interfering - genetics Tumor Burden - drug effects Tumors Up-Regulation |
| Title | 17β‐estradiol upregulates GREB1 and accelerates ovarian tumor progression in vivo |
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