G protein-coupled estrogen receptor 1 (GPER-1) and agonist G-1 inhibit growth of ovarian cancer cells by activation of anti-tumoral transcriptome responses: impact of GPER-1 mRNA on survival
Purpose The present study intended to further elucidate the role of G protein-coupled estrogen receptor 1 (GPER-1) in ovarian cancer by comparing the effects of a GPER-1 knockdown and treatment with its agonist G-1 on cell growth, apoptosis, and the transcriptome of two ovarian cancer cell lines. Fu...
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| Veröffentlicht in: | Journal of cancer research and clinical oncology 2020-12, Vol.146 (12), p.3175-3188 |
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| container_title | Journal of cancer research and clinical oncology |
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| creator | Schüler-Toprak, Susanne Skrzypczak, Maciej Ignatov, Tanja Ignatov, Atanas Ortmann, Olaf Treeck, Oliver |
| description | Purpose
The present study intended to further elucidate the role of G protein-coupled estrogen receptor 1 (GPER-1) in ovarian cancer by comparing the effects of a GPER-1 knockdown and treatment with its agonist G-1 on cell growth, apoptosis, and the transcriptome of two ovarian cancer cell lines. Furthermore, the role of GPER-1 in ovarian cancer survival was examined.
Methods
GPER-1 expression in OVCAR-3 and OAW-42 ovarian cancer cells was knocked down by RNAi. The effects on cell growth were measured by means of the fluorimetric cell titer blue assay and on the transcriptome by Affymetrix GeneChip analysis. The effect of GPER-1 on patient’s survival was examined using open source mRNA and clinical data of 1657 ovarian cancer patients.
Results
GPER-1 knockdown resulted in a significant growth stimulation of both cell lines, whereas treatment with agonist G-1 decreased growth of both cell lines in a dose-dependent manner. Transcriptome analyses revealed a set of 18 genes being conversely regulated after GPER-1 knockdown and G-1 treatment. Generally, treatment with G-1 led to a transcriptome response associated with growth inhibition. In contrast, knockdown of GPER-1 exerted opposite effects, stimulating pathways activating mitosis, but inhibiting pathways associated with apoptosis or interferon signaling. Further analyses using open-access mRNA and clinical data by bioinformatical online tools revealed a longer OS (HR = 0.86,
p
= 0.057) and PFS (HR = 0.81,
p
= 0.0035) of ovarian cancer patients with high GPER-1 mRNA expression.
Conclusions
The results of this study clearly support the hypothesis that GPER-1 acts as a tumor suppressor in ovarian cancer. |
| doi_str_mv | 10.1007/s00432-020-03333-4 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2473319281</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2473319281</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-787efbddce2c4d4a9686c61b40a7e26711d18be8d97d05789d9b7dcd9bb70fef3</originalsourceid><addsrcrecordid>eNp9UU2P1SAUJUbjPJ_-ARfmJm50gUJpS-tuMhmfJhM1E103FG7fMGmhAn1m_py_TWpH3cniErjnIzmHkOecveGMybeRsVIUlBWMMpEPLR-QHV-_uBDVQ7JjXHJaFbw-I09ivGX5XcniMTkTRcMF59WO_DzAHHxC66j2yzyiAYwp-CM6CKhxTj4Ah1eHL5fXlL8G5Qyoo3c2JjhQDtbd2N4mOAb_I92AH8CfVLDKgVZOYwCN4xihvwOlkz2pZL1bUcolS9My-aBGSEG5qIPNZhNm2zh7FzG-AzvNmbbiN3-Yrj-dQ1aISzhltfEpeTSoMeKz-3tPvr2__HrxgV59Pny8OL-iWsgqUdlIHHpjNBa6NKVq66bWNe9LpiQWteTc8KbHxrTSsEo2rWl7aXSevWQDDmJPXm66OazvS06ou_VLcNmyK0opBG_XRPek2FA6-BgDDt0c7KTCXcdZt1bWbZV1ubLud2VdmUkv7qWXfkLzl_KnowwQGyDmlTti-Of9H9lf2PGjlA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2473319281</pqid></control><display><type>article</type><title>G protein-coupled estrogen receptor 1 (GPER-1) and agonist G-1 inhibit growth of ovarian cancer cells by activation of anti-tumoral transcriptome responses: impact of GPER-1 mRNA on survival</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Schüler-Toprak, Susanne ; Skrzypczak, Maciej ; Ignatov, Tanja ; Ignatov, Atanas ; Ortmann, Olaf ; Treeck, Oliver</creator><creatorcontrib>Schüler-Toprak, Susanne ; Skrzypczak, Maciej ; Ignatov, Tanja ; Ignatov, Atanas ; Ortmann, Olaf ; Treeck, Oliver</creatorcontrib><description>Purpose
The present study intended to further elucidate the role of G protein-coupled estrogen receptor 1 (GPER-1) in ovarian cancer by comparing the effects of a GPER-1 knockdown and treatment with its agonist G-1 on cell growth, apoptosis, and the transcriptome of two ovarian cancer cell lines. Furthermore, the role of GPER-1 in ovarian cancer survival was examined.
Methods
GPER-1 expression in OVCAR-3 and OAW-42 ovarian cancer cells was knocked down by RNAi. The effects on cell growth were measured by means of the fluorimetric cell titer blue assay and on the transcriptome by Affymetrix GeneChip analysis. The effect of GPER-1 on patient’s survival was examined using open source mRNA and clinical data of 1657 ovarian cancer patients.
Results
GPER-1 knockdown resulted in a significant growth stimulation of both cell lines, whereas treatment with agonist G-1 decreased growth of both cell lines in a dose-dependent manner. Transcriptome analyses revealed a set of 18 genes being conversely regulated after GPER-1 knockdown and G-1 treatment. Generally, treatment with G-1 led to a transcriptome response associated with growth inhibition. In contrast, knockdown of GPER-1 exerted opposite effects, stimulating pathways activating mitosis, but inhibiting pathways associated with apoptosis or interferon signaling. Further analyses using open-access mRNA and clinical data by bioinformatical online tools revealed a longer OS (HR = 0.86,
p
= 0.057) and PFS (HR = 0.81,
p
= 0.0035) of ovarian cancer patients with high GPER-1 mRNA expression.
Conclusions
The results of this study clearly support the hypothesis that GPER-1 acts as a tumor suppressor in ovarian cancer.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-020-03333-4</identifier><identifier>PMID: 32813115</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Agonists ; Apoptosis ; Apoptosis - drug effects ; Cancer Research ; Cell activation ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - genetics ; Cyclopentanes - pharmacology ; Estrogen receptors ; Estrogens ; Female ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic - drug effects ; Hematology ; Humans ; Interferon ; Internal Medicine ; Medicine ; Medicine & Public Health ; Mitosis ; Oncology ; Original Article – Cancer Research ; Ovarian cancer ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - pathology ; Patients ; Quinolines - pharmacology ; Receptors, Estrogen - genetics ; Receptors, G-Protein-Coupled - genetics ; RNA, Messenger - genetics ; RNA-mediated interference ; Transcriptome - genetics ; Tumor cell lines ; Tumor suppressor genes</subject><ispartof>Journal of cancer research and clinical oncology, 2020-12, Vol.146 (12), p.3175-3188</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020</rights><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-787efbddce2c4d4a9686c61b40a7e26711d18be8d97d05789d9b7dcd9bb70fef3</citedby><cites>FETCH-LOGICAL-c375t-787efbddce2c4d4a9686c61b40a7e26711d18be8d97d05789d9b7dcd9bb70fef3</cites><orcidid>0000-0003-2353-9693</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00432-020-03333-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-020-03333-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32813115$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schüler-Toprak, Susanne</creatorcontrib><creatorcontrib>Skrzypczak, Maciej</creatorcontrib><creatorcontrib>Ignatov, Tanja</creatorcontrib><creatorcontrib>Ignatov, Atanas</creatorcontrib><creatorcontrib>Ortmann, Olaf</creatorcontrib><creatorcontrib>Treeck, Oliver</creatorcontrib><title>G protein-coupled estrogen receptor 1 (GPER-1) and agonist G-1 inhibit growth of ovarian cancer cells by activation of anti-tumoral transcriptome responses: impact of GPER-1 mRNA on survival</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Purpose
The present study intended to further elucidate the role of G protein-coupled estrogen receptor 1 (GPER-1) in ovarian cancer by comparing the effects of a GPER-1 knockdown and treatment with its agonist G-1 on cell growth, apoptosis, and the transcriptome of two ovarian cancer cell lines. Furthermore, the role of GPER-1 in ovarian cancer survival was examined.
Methods
GPER-1 expression in OVCAR-3 and OAW-42 ovarian cancer cells was knocked down by RNAi. The effects on cell growth were measured by means of the fluorimetric cell titer blue assay and on the transcriptome by Affymetrix GeneChip analysis. The effect of GPER-1 on patient’s survival was examined using open source mRNA and clinical data of 1657 ovarian cancer patients.
Results
GPER-1 knockdown resulted in a significant growth stimulation of both cell lines, whereas treatment with agonist G-1 decreased growth of both cell lines in a dose-dependent manner. Transcriptome analyses revealed a set of 18 genes being conversely regulated after GPER-1 knockdown and G-1 treatment. Generally, treatment with G-1 led to a transcriptome response associated with growth inhibition. In contrast, knockdown of GPER-1 exerted opposite effects, stimulating pathways activating mitosis, but inhibiting pathways associated with apoptosis or interferon signaling. Further analyses using open-access mRNA and clinical data by bioinformatical online tools revealed a longer OS (HR = 0.86,
p
= 0.057) and PFS (HR = 0.81,
p
= 0.0035) of ovarian cancer patients with high GPER-1 mRNA expression.
Conclusions
The results of this study clearly support the hypothesis that GPER-1 acts as a tumor suppressor in ovarian cancer.</description><subject>Agonists</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Cancer Research</subject><subject>Cell activation</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Cyclopentanes - pharmacology</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Hematology</subject><subject>Humans</subject><subject>Interferon</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mitosis</subject><subject>Oncology</subject><subject>Original Article – Cancer Research</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Patients</subject><subject>Quinolines - pharmacology</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, G-Protein-Coupled - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>RNA-mediated interference</subject><subject>Transcriptome - genetics</subject><subject>Tumor cell lines</subject><subject>Tumor suppressor genes</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9UU2P1SAUJUbjPJ_-ARfmJm50gUJpS-tuMhmfJhM1E103FG7fMGmhAn1m_py_TWpH3cniErjnIzmHkOecveGMybeRsVIUlBWMMpEPLR-QHV-_uBDVQ7JjXHJaFbw-I09ivGX5XcniMTkTRcMF59WO_DzAHHxC66j2yzyiAYwp-CM6CKhxTj4Ah1eHL5fXlL8G5Qyoo3c2JjhQDtbd2N4mOAb_I92AH8CfVLDKgVZOYwCN4xihvwOlkz2pZL1bUcolS9My-aBGSEG5qIPNZhNm2zh7FzG-AzvNmbbiN3-Yrj-dQ1aISzhltfEpeTSoMeKz-3tPvr2__HrxgV59Pny8OL-iWsgqUdlIHHpjNBa6NKVq66bWNe9LpiQWteTc8KbHxrTSsEo2rWl7aXSevWQDDmJPXm66OazvS06ou_VLcNmyK0opBG_XRPek2FA6-BgDDt0c7KTCXcdZt1bWbZV1ubLud2VdmUkv7qWXfkLzl_KnowwQGyDmlTti-Of9H9lf2PGjlA</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Schüler-Toprak, Susanne</creator><creator>Skrzypczak, Maciej</creator><creator>Ignatov, Tanja</creator><creator>Ignatov, Atanas</creator><creator>Ortmann, Olaf</creator><creator>Treeck, Oliver</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><orcidid>https://orcid.org/0000-0003-2353-9693</orcidid></search><sort><creationdate>20201201</creationdate><title>G protein-coupled estrogen receptor 1 (GPER-1) and agonist G-1 inhibit growth of ovarian cancer cells by activation of anti-tumoral transcriptome responses: impact of GPER-1 mRNA on survival</title><author>Schüler-Toprak, Susanne ; Skrzypczak, Maciej ; Ignatov, Tanja ; Ignatov, Atanas ; Ortmann, Olaf ; Treeck, Oliver</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-787efbddce2c4d4a9686c61b40a7e26711d18be8d97d05789d9b7dcd9bb70fef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Agonists</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Cancer Research</topic><topic>Cell activation</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Cyclopentanes - pharmacology</topic><topic>Estrogen receptors</topic><topic>Estrogens</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Hematology</topic><topic>Humans</topic><topic>Interferon</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mitosis</topic><topic>Oncology</topic><topic>Original Article – Cancer Research</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - drug therapy</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Patients</topic><topic>Quinolines - pharmacology</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, G-Protein-Coupled - genetics</topic><topic>RNA, Messenger - genetics</topic><topic>RNA-mediated interference</topic><topic>Transcriptome - genetics</topic><topic>Tumor cell lines</topic><topic>Tumor suppressor genes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schüler-Toprak, Susanne</creatorcontrib><creatorcontrib>Skrzypczak, Maciej</creatorcontrib><creatorcontrib>Ignatov, Tanja</creatorcontrib><creatorcontrib>Ignatov, Atanas</creatorcontrib><creatorcontrib>Ortmann, Olaf</creatorcontrib><creatorcontrib>Treeck, Oliver</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schüler-Toprak, Susanne</au><au>Skrzypczak, Maciej</au><au>Ignatov, Tanja</au><au>Ignatov, Atanas</au><au>Ortmann, Olaf</au><au>Treeck, Oliver</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>G protein-coupled estrogen receptor 1 (GPER-1) and agonist G-1 inhibit growth of ovarian cancer cells by activation of anti-tumoral transcriptome responses: impact of GPER-1 mRNA on survival</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>146</volume><issue>12</issue><spage>3175</spage><epage>3188</epage><pages>3175-3188</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>Purpose
The present study intended to further elucidate the role of G protein-coupled estrogen receptor 1 (GPER-1) in ovarian cancer by comparing the effects of a GPER-1 knockdown and treatment with its agonist G-1 on cell growth, apoptosis, and the transcriptome of two ovarian cancer cell lines. Furthermore, the role of GPER-1 in ovarian cancer survival was examined.
Methods
GPER-1 expression in OVCAR-3 and OAW-42 ovarian cancer cells was knocked down by RNAi. The effects on cell growth were measured by means of the fluorimetric cell titer blue assay and on the transcriptome by Affymetrix GeneChip analysis. The effect of GPER-1 on patient’s survival was examined using open source mRNA and clinical data of 1657 ovarian cancer patients.
Results
GPER-1 knockdown resulted in a significant growth stimulation of both cell lines, whereas treatment with agonist G-1 decreased growth of both cell lines in a dose-dependent manner. Transcriptome analyses revealed a set of 18 genes being conversely regulated after GPER-1 knockdown and G-1 treatment. Generally, treatment with G-1 led to a transcriptome response associated with growth inhibition. In contrast, knockdown of GPER-1 exerted opposite effects, stimulating pathways activating mitosis, but inhibiting pathways associated with apoptosis or interferon signaling. Further analyses using open-access mRNA and clinical data by bioinformatical online tools revealed a longer OS (HR = 0.86,
p
= 0.057) and PFS (HR = 0.81,
p
= 0.0035) of ovarian cancer patients with high GPER-1 mRNA expression.
Conclusions
The results of this study clearly support the hypothesis that GPER-1 acts as a tumor suppressor in ovarian cancer.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>32813115</pmid><doi>10.1007/s00432-020-03333-4</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-2353-9693</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0171-5216 |
| ispartof | Journal of cancer research and clinical oncology, 2020-12, Vol.146 (12), p.3175-3188 |
| issn | 0171-5216 1432-1335 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Agonists Apoptosis Apoptosis - drug effects Cancer Research Cell activation Cell growth Cell Line, Tumor Cell Proliferation - genetics Cyclopentanes - pharmacology Estrogen receptors Estrogens Female Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic - drug effects Hematology Humans Interferon Internal Medicine Medicine Medicine & Public Health Mitosis Oncology Original Article – Cancer Research Ovarian cancer Ovarian Neoplasms - drug therapy Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Patients Quinolines - pharmacology Receptors, Estrogen - genetics Receptors, G-Protein-Coupled - genetics RNA, Messenger - genetics RNA-mediated interference Transcriptome - genetics Tumor cell lines Tumor suppressor genes |
| title | G protein-coupled estrogen receptor 1 (GPER-1) and agonist G-1 inhibit growth of ovarian cancer cells by activation of anti-tumoral transcriptome responses: impact of GPER-1 mRNA on survival |
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