17β-Estradiol sensitizes ovarian surface epithelium to transformation by suppressing Disabled-2 expression
Estrogen replacement therapy increases the risk of human ovarian cancer and exogenous estradiol accelerates the onset of ovarian cancer in mouse models. This study uses primary cultures of mouse ovarian surface epithelium (OSE) to demonstrate that one possible mechanism by which estrogen accelerates...
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| Abstract | Estrogen replacement therapy increases the risk of human ovarian cancer and exogenous estradiol accelerates the onset of ovarian cancer in mouse models. This study uses primary cultures of mouse ovarian surface epithelium (OSE) to demonstrate that one possible mechanism by which estrogen accelerates the initiation of ovarian cancer is by up-regulation of microRNA-378 via the ESR1 pathway to result in the down-regulation of a tumour suppressor called
Disabled-2
(
Dab2
). Estrogen suppression of
Dab2
was reproducible
in vivo
and across many cell types including mouse oviductal epithelium and primary cultures of human ovarian cancer cells. Suppression of
Dab2
resulted in increased proliferation, loss of contact inhibition, morphological dysplasia, and resistance to oncogene-induced senescence – all factors that can sensitize OSE to transformation. Given that
DAB2
is highly expressed in healthy human OSE and is absent in the majority of ovarian tumours, this study has taken the first steps to provide a mechanistic explanation for how estrogen therapy may play a role in the initiation of ovarian cancer. |
|---|---|
| AbstractList | Estrogen replacement therapy increases the risk of human ovarian cancer and exogenous estradiol accelerates the onset of ovarian cancer in mouse models. This study uses primary cultures of mouse ovarian surface epithelium (OSE) to demonstrate that one possible mechanism by which estrogen accelerates the initiation of ovarian cancer is by up-regulation of microRNA-378 via the ESR1 pathway to result in the down-regulation of a tumour suppressor called
Disabled-2
(
Dab2
). Estrogen suppression of
Dab2
was reproducible
in vivo
and across many cell types including mouse oviductal epithelium and primary cultures of human ovarian cancer cells. Suppression of
Dab2
resulted in increased proliferation, loss of contact inhibition, morphological dysplasia, and resistance to oncogene-induced senescence – all factors that can sensitize OSE to transformation. Given that
DAB2
is highly expressed in healthy human OSE and is absent in the majority of ovarian tumours, this study has taken the first steps to provide a mechanistic explanation for how estrogen therapy may play a role in the initiation of ovarian cancer. Estrogen replacement therapy increases the risk of human ovarian cancer and exogenous estradiol accelerates the onset of ovarian cancer in mouse models. This study uses primary cultures of mouse ovarian surface epithelium (OSE) to demonstrate that one possible mechanism by which estrogen accelerates the initiation of ovarian cancer is by up-regulation of microRNA-378 via the ESR1 pathway to result in the down-regulation of a tumour suppressor called Disabled-2 (Dab2). Estrogen suppression of Dab2 was reproducible in vivo and across many cell types including mouse oviductal epithelium and primary cultures of human ovarian cancer cells. Suppression of Dab2 resulted in increased proliferation, loss of contact inhibition, morphological dysplasia, and resistance to oncogene-induced senescence - all factors that can sensitize OSE to transformation. Given that DAB2 is highly expressed in healthy human OSE and is absent in the majority of ovarian tumours, this study has taken the first steps to provide a mechanistic explanation for how estrogen therapy may play a role in the initiation of ovarian cancer. Estrogen replacement therapy increases the risk of human ovarian cancer and exogenous estradiol accelerates the onset of ovarian cancer in mouse models. This study uses primary cultures of mouse ovarian surface epithelium (OSE) to demonstrate that one possible mechanism by which estrogen accelerates the initiation of ovarian cancer is by up-regulation of microRNA-378 via the ESR1 pathway to result in the down-regulation of a tumour suppressor called Disabled-2 (Dab2). Estrogen suppression of Dab2 was reproducible in vivo and across many cell types including mouse oviductal epithelium and primary cultures of human ovarian cancer cells. Suppression of Dab2 resulted in increased proliferation, loss of contact inhibition, morphological dysplasia, and resistance to oncogene-induced senescence - all factors that can sensitize OSE to transformation. Given that DAB2 is highly expressed in healthy human OSE and is absent in the majority of ovarian tumours, this study has taken the first steps to provide a mechanistic explanation for how estrogen therapy may play a role in the initiation of ovarian cancer.Estrogen replacement therapy increases the risk of human ovarian cancer and exogenous estradiol accelerates the onset of ovarian cancer in mouse models. This study uses primary cultures of mouse ovarian surface epithelium (OSE) to demonstrate that one possible mechanism by which estrogen accelerates the initiation of ovarian cancer is by up-regulation of microRNA-378 via the ESR1 pathway to result in the down-regulation of a tumour suppressor called Disabled-2 (Dab2). Estrogen suppression of Dab2 was reproducible in vivo and across many cell types including mouse oviductal epithelium and primary cultures of human ovarian cancer cells. Suppression of Dab2 resulted in increased proliferation, loss of contact inhibition, morphological dysplasia, and resistance to oncogene-induced senescence - all factors that can sensitize OSE to transformation. Given that DAB2 is highly expressed in healthy human OSE and is absent in the majority of ovarian tumours, this study has taken the first steps to provide a mechanistic explanation for how estrogen therapy may play a role in the initiation of ovarian cancer. |
| ArticleNumber | 16702 |
| Author | Vanderhyden, Barbara C. Vuong, Nhung H. Salah Salah, Omar |
| Author_xml | – sequence: 1 givenname: Nhung H. surname: Vuong fullname: Vuong, Nhung H. organization: Department of Cellular and Molecular Medicine, University of Ottawa, Cancer Therapeutics Program, Ottawa Hospital Research Institute – sequence: 2 givenname: Omar surname: Salah Salah fullname: Salah Salah, Omar organization: Cancer Therapeutics Program, Ottawa Hospital Research Institute – sequence: 3 givenname: Barbara C. surname: Vanderhyden fullname: Vanderhyden, Barbara C. email: bvanderhyden@ohri.ca organization: Department of Cellular and Molecular Medicine, University of Ottawa, Cancer Therapeutics Program, Ottawa Hospital Research Institute |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29196616$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1093_biolre_ioz134 crossref_primary_10_1038_s41598_020_66559_9 crossref_primary_10_3390_ijms24010696 crossref_primary_10_1371_journal_pgen_1007788 crossref_primary_10_1007_s11033_024_09653_9 crossref_primary_10_3390_molecules25215214 crossref_primary_10_1002_mco2_475 crossref_primary_10_1093_molehr_gaad006 |
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| Title | 17β-Estradiol sensitizes ovarian surface epithelium to transformation by suppressing Disabled-2 expression |
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