Estrogen and aryl hydrocarbon receptor expression and crosstalk in human Ishikawa endometrial cancer cells
Ishikawa endometrial cancer cells express the estrogen receptor (ER), and this study investigates aryl hydrocarbon receptor (AhR) expression and inhibitory AhR–ER crosstalk in this cell line. Treatment of Ishikawa cells with the AhR agonist [ 3H]2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) gave a rad...
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| Veröffentlicht in: | The Journal of steroid biochemistry and molecular biology 2000-04, Vol.72 (5), p.197-207 |
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| creator | Wormke, Mark Castro-Rivera, Emely Chen, Ichen Safe, Stephen |
| description | Ishikawa endometrial cancer cells express the estrogen receptor (ER), and this study investigates aryl hydrocarbon receptor (AhR) expression and inhibitory AhR–ER crosstalk in this cell line. Treatment of Ishikawa cells with the AhR agonist [
3H]2,3,7,8-tetrachlorodibenzo-
p-dioxin (TCDD) gave a radiolabeled nuclear complex that sedimented at 6.0 S in sucrose density gradients, and Western blot analysis confirmed that Ishikawa cells expressed human AhR and AhR nuclear translocator (Arnt) proteins. Treatment of Ishikawa cells with 10 nM TCDD induced a 9.7-fold increase in CYP1A1-dependent ethoxyresorufin
O-deethylase (EROD) activity and a 10.5-fold increase in chloramphenicol acetyltransferase (CAT) activity in cells transfected with pRNH11c containing an Ah-responsive human CYP1A1 gene promoter insert (−1142 to +2434). Inhibitory AhR–ER crosstalk was investigated in Ishikawa cells using E2-induced cell proliferation and transcriptional activation assays in cells transfected with E2-responsive constructs containing promoter inserts from the progesterone receptor and vitellogenin A2 genes. AhR agonists including TCDD, benzo[a]pyrene (BaP) and 6-methyl-1,3,8-trichlorodibenzofuran, inhibited 32–47% of the E2-induced responses. In contrast, neither estrogen nor progesterone inhibited EROD activity induced by TCDD in Ishikawa cells, whereas inhibitory ER-AhR crosstalk was observed in ECC-1 endometrial cells suggesting that these interactions were cell context-dependent. |
| doi_str_mv | 10.1016/S0960-0760(00)00030-3 |
| format | Article |
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3H]2,3,7,8-tetrachlorodibenzo-
p-dioxin (TCDD) gave a radiolabeled nuclear complex that sedimented at 6.0 S in sucrose density gradients, and Western blot analysis confirmed that Ishikawa cells expressed human AhR and AhR nuclear translocator (Arnt) proteins. Treatment of Ishikawa cells with 10 nM TCDD induced a 9.7-fold increase in CYP1A1-dependent ethoxyresorufin
O-deethylase (EROD) activity and a 10.5-fold increase in chloramphenicol acetyltransferase (CAT) activity in cells transfected with pRNH11c containing an Ah-responsive human CYP1A1 gene promoter insert (−1142 to +2434). Inhibitory AhR–ER crosstalk was investigated in Ishikawa cells using E2-induced cell proliferation and transcriptional activation assays in cells transfected with E2-responsive constructs containing promoter inserts from the progesterone receptor and vitellogenin A2 genes. AhR agonists including TCDD, benzo[a]pyrene (BaP) and 6-methyl-1,3,8-trichlorodibenzofuran, inhibited 32–47% of the E2-induced responses. In contrast, neither estrogen nor progesterone inhibited EROD activity induced by TCDD in Ishikawa cells, whereas inhibitory ER-AhR crosstalk was observed in ECC-1 endometrial cells suggesting that these interactions were cell context-dependent.</description><identifier>ISSN: 0960-0760</identifier><identifier>EISSN: 1879-1220</identifier><identifier>DOI: 10.1016/S0960-0760(00)00030-3</identifier><identifier>PMID: 10822009</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - genetics ; Adenocarcinoma - metabolism ; Aryl Hydrocarbon Receptor Nuclear Translocator ; aryl hydrocarbon receptors ; Benzo(a)pyrene - pharmacology ; Benzofurans - pharmacology ; Biological and medical sciences ; Chloramphenicol O-Acetyltransferase - drug effects ; Chloramphenicol O-Acetyltransferase - genetics ; Chloramphenicol O-Acetyltransferase - metabolism ; Cytochrome P-450 CYP1A1 - drug effects ; Cytochrome P-450 CYP1A1 - genetics ; Cytochrome P-450 CYP1A1 - metabolism ; DNA-Binding Proteins ; Endometrial Neoplasms - drug therapy ; Endometrial Neoplasms - genetics ; Endometrial Neoplasms - metabolism ; Estradiol - pharmacology ; Female ; Female genital diseases ; Gynecology. Andrology. Obstetrics ; Humans ; Medical sciences ; Polychlorinated Dibenzodioxins - pharmacology ; Promoter Regions, Genetic ; Receptors, Aryl Hydrocarbon - agonists ; Receptors, Aryl Hydrocarbon - genetics ; Receptors, Aryl Hydrocarbon - metabolism ; Receptors, Estrogen - drug effects ; Receptors, Estrogen - genetics ; Receptors, Estrogen - metabolism ; Receptors, Progesterone - drug effects ; Receptors, Progesterone - genetics ; Receptors, Progesterone - metabolism ; Transcription Factors - drug effects ; Transcription Factors - metabolism ; Transcription, Genetic ; Tumor Cells, Cultured ; Tumors</subject><ispartof>The Journal of steroid biochemistry and molecular biology, 2000-04, Vol.72 (5), p.197-207</ispartof><rights>2000 Elsevier Science Ltd</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-92fcd7fe882d12317cc4112fa3476d27848d187e906c2975c2ac493e8b3eef133</citedby><cites>FETCH-LOGICAL-c421t-92fcd7fe882d12317cc4112fa3476d27848d187e906c2975c2ac493e8b3eef133</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0960-0760(00)00030-3$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1440845$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10822009$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wormke, Mark</creatorcontrib><creatorcontrib>Castro-Rivera, Emely</creatorcontrib><creatorcontrib>Chen, Ichen</creatorcontrib><creatorcontrib>Safe, Stephen</creatorcontrib><title>Estrogen and aryl hydrocarbon receptor expression and crosstalk in human Ishikawa endometrial cancer cells</title><title>The Journal of steroid biochemistry and molecular biology</title><addtitle>J Steroid Biochem Mol Biol</addtitle><description>Ishikawa endometrial cancer cells express the estrogen receptor (ER), and this study investigates aryl hydrocarbon receptor (AhR) expression and inhibitory AhR–ER crosstalk in this cell line. Treatment of Ishikawa cells with the AhR agonist [
3H]2,3,7,8-tetrachlorodibenzo-
p-dioxin (TCDD) gave a radiolabeled nuclear complex that sedimented at 6.0 S in sucrose density gradients, and Western blot analysis confirmed that Ishikawa cells expressed human AhR and AhR nuclear translocator (Arnt) proteins. Treatment of Ishikawa cells with 10 nM TCDD induced a 9.7-fold increase in CYP1A1-dependent ethoxyresorufin
O-deethylase (EROD) activity and a 10.5-fold increase in chloramphenicol acetyltransferase (CAT) activity in cells transfected with pRNH11c containing an Ah-responsive human CYP1A1 gene promoter insert (−1142 to +2434). Inhibitory AhR–ER crosstalk was investigated in Ishikawa cells using E2-induced cell proliferation and transcriptional activation assays in cells transfected with E2-responsive constructs containing promoter inserts from the progesterone receptor and vitellogenin A2 genes. AhR agonists including TCDD, benzo[a]pyrene (BaP) and 6-methyl-1,3,8-trichlorodibenzofuran, inhibited 32–47% of the E2-induced responses. In contrast, neither estrogen nor progesterone inhibited EROD activity induced by TCDD in Ishikawa cells, whereas inhibitory ER-AhR crosstalk was observed in ECC-1 endometrial cells suggesting that these interactions were cell context-dependent.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - metabolism</subject><subject>Aryl Hydrocarbon Receptor Nuclear Translocator</subject><subject>aryl hydrocarbon receptors</subject><subject>Benzo(a)pyrene - pharmacology</subject><subject>Benzofurans - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Chloramphenicol O-Acetyltransferase - drug effects</subject><subject>Chloramphenicol O-Acetyltransferase - genetics</subject><subject>Chloramphenicol O-Acetyltransferase - metabolism</subject><subject>Cytochrome P-450 CYP1A1 - drug effects</subject><subject>Cytochrome P-450 CYP1A1 - genetics</subject><subject>Cytochrome P-450 CYP1A1 - metabolism</subject><subject>DNA-Binding Proteins</subject><subject>Endometrial Neoplasms - drug therapy</subject><subject>Endometrial Neoplasms - genetics</subject><subject>Endometrial Neoplasms - metabolism</subject><subject>Estradiol - pharmacology</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Polychlorinated Dibenzodioxins - pharmacology</subject><subject>Promoter Regions, Genetic</subject><subject>Receptors, Aryl Hydrocarbon - agonists</subject><subject>Receptors, Aryl Hydrocarbon - genetics</subject><subject>Receptors, Aryl Hydrocarbon - metabolism</subject><subject>Receptors, Estrogen - drug effects</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Receptors, Progesterone - drug effects</subject><subject>Receptors, Progesterone - genetics</subject><subject>Receptors, Progesterone - metabolism</subject><subject>Transcription Factors - drug effects</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription, Genetic</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0960-0760</issn><issn>1879-1220</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1O3DAURq2qqAzTPgKVF1VFF2mvfxInK4QQUCQkFm3Xlse-YQxJPLUzFN4eh4wKOyRL3pxrf_d8hBwy-M6AVT9-QVNBAaqCI4BvACCgEO_IgtWqKRjn8J4s_iP75CCl2wkSTH0g-wzqTECzILdnaYzhBgdqBkdNfOzo-tHFYE1chYFGtLgZQ6T4sImYkg8zaGNIaTTdHfUDXW97M9DLtPZ35p-hOLjQ4xi96ag1g8VILXZd-kj2WtMl_LS7l-TP-dnv05_F1fXF5enJVWElZ2PR8NY61WJdc8d4zmutZIy3RkhVOa5qWbu8JDZQWd6o0nJjZSOwXgnElgmxJF_ndzcx_N1iGnXv05TADBi2SSvGBM9m3gSZKmU5OVuScgaf147Y6k30fZalGeipDf3chp5Ua5hObkNPc593H2xXPbpXU7P-DHzZASZZ07Ux6_LphZMSallm7HjGMGu79xh1sh6zWedzQaN2wb-R5Al8Mqbm</recordid><startdate>20000401</startdate><enddate>20000401</enddate><creator>Wormke, Mark</creator><creator>Castro-Rivera, Emely</creator><creator>Chen, Ichen</creator><creator>Safe, Stephen</creator><general>Elsevier Ltd</general><general>Elsevier Science</general><scope>IQODW</scope><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>7TM</scope><scope>7X8</scope></search><sort><creationdate>20000401</creationdate><title>Estrogen and aryl hydrocarbon receptor expression and crosstalk in human Ishikawa endometrial cancer cells</title><author>Wormke, Mark ; Castro-Rivera, Emely ; Chen, Ichen ; Safe, Stephen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-92fcd7fe882d12317cc4112fa3476d27848d187e906c2975c2ac493e8b3eef133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - metabolism</topic><topic>Aryl Hydrocarbon Receptor Nuclear Translocator</topic><topic>aryl hydrocarbon receptors</topic><topic>Benzo(a)pyrene - pharmacology</topic><topic>Benzofurans - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Chloramphenicol O-Acetyltransferase - drug effects</topic><topic>Chloramphenicol O-Acetyltransferase - genetics</topic><topic>Chloramphenicol O-Acetyltransferase - metabolism</topic><topic>Cytochrome P-450 CYP1A1 - drug effects</topic><topic>Cytochrome P-450 CYP1A1 - genetics</topic><topic>Cytochrome P-450 CYP1A1 - metabolism</topic><topic>DNA-Binding Proteins</topic><topic>Endometrial Neoplasms - drug therapy</topic><topic>Endometrial Neoplasms - genetics</topic><topic>Endometrial Neoplasms - metabolism</topic><topic>Estradiol - pharmacology</topic><topic>Female</topic><topic>Female genital diseases</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Polychlorinated Dibenzodioxins - pharmacology</topic><topic>Promoter Regions, Genetic</topic><topic>Receptors, Aryl Hydrocarbon - agonists</topic><topic>Receptors, Aryl Hydrocarbon - genetics</topic><topic>Receptors, Aryl Hydrocarbon - metabolism</topic><topic>Receptors, Estrogen - drug effects</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Receptors, Progesterone - drug effects</topic><topic>Receptors, Progesterone - genetics</topic><topic>Receptors, Progesterone - metabolism</topic><topic>Transcription Factors - drug effects</topic><topic>Transcription Factors - metabolism</topic><topic>Transcription, Genetic</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wormke, Mark</creatorcontrib><creatorcontrib>Castro-Rivera, Emely</creatorcontrib><creatorcontrib>Chen, Ichen</creatorcontrib><creatorcontrib>Safe, Stephen</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wormke, Mark</au><au>Castro-Rivera, Emely</au><au>Chen, Ichen</au><au>Safe, Stephen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Estrogen and aryl hydrocarbon receptor expression and crosstalk in human Ishikawa endometrial cancer cells</atitle><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle><addtitle>J Steroid Biochem Mol Biol</addtitle><date>2000-04-01</date><risdate>2000</risdate><volume>72</volume><issue>5</issue><spage>197</spage><epage>207</epage><pages>197-207</pages><issn>0960-0760</issn><eissn>1879-1220</eissn><abstract>Ishikawa endometrial cancer cells express the estrogen receptor (ER), and this study investigates aryl hydrocarbon receptor (AhR) expression and inhibitory AhR–ER crosstalk in this cell line. Treatment of Ishikawa cells with the AhR agonist [
3H]2,3,7,8-tetrachlorodibenzo-
p-dioxin (TCDD) gave a radiolabeled nuclear complex that sedimented at 6.0 S in sucrose density gradients, and Western blot analysis confirmed that Ishikawa cells expressed human AhR and AhR nuclear translocator (Arnt) proteins. Treatment of Ishikawa cells with 10 nM TCDD induced a 9.7-fold increase in CYP1A1-dependent ethoxyresorufin
O-deethylase (EROD) activity and a 10.5-fold increase in chloramphenicol acetyltransferase (CAT) activity in cells transfected with pRNH11c containing an Ah-responsive human CYP1A1 gene promoter insert (−1142 to +2434). Inhibitory AhR–ER crosstalk was investigated in Ishikawa cells using E2-induced cell proliferation and transcriptional activation assays in cells transfected with E2-responsive constructs containing promoter inserts from the progesterone receptor and vitellogenin A2 genes. AhR agonists including TCDD, benzo[a]pyrene (BaP) and 6-methyl-1,3,8-trichlorodibenzofuran, inhibited 32–47% of the E2-induced responses. In contrast, neither estrogen nor progesterone inhibited EROD activity induced by TCDD in Ishikawa cells, whereas inhibitory ER-AhR crosstalk was observed in ECC-1 endometrial cells suggesting that these interactions were cell context-dependent.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>10822009</pmid><doi>10.1016/S0960-0760(00)00030-3</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0960-0760 |
| ispartof | The Journal of steroid biochemistry and molecular biology, 2000-04, Vol.72 (5), p.197-207 |
| issn | 0960-0760 1879-1220 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Adenocarcinoma - drug therapy Adenocarcinoma - genetics Adenocarcinoma - metabolism Aryl Hydrocarbon Receptor Nuclear Translocator aryl hydrocarbon receptors Benzo(a)pyrene - pharmacology Benzofurans - pharmacology Biological and medical sciences Chloramphenicol O-Acetyltransferase - drug effects Chloramphenicol O-Acetyltransferase - genetics Chloramphenicol O-Acetyltransferase - metabolism Cytochrome P-450 CYP1A1 - drug effects Cytochrome P-450 CYP1A1 - genetics Cytochrome P-450 CYP1A1 - metabolism DNA-Binding Proteins Endometrial Neoplasms - drug therapy Endometrial Neoplasms - genetics Endometrial Neoplasms - metabolism Estradiol - pharmacology Female Female genital diseases Gynecology. Andrology. Obstetrics Humans Medical sciences Polychlorinated Dibenzodioxins - pharmacology Promoter Regions, Genetic Receptors, Aryl Hydrocarbon - agonists Receptors, Aryl Hydrocarbon - genetics Receptors, Aryl Hydrocarbon - metabolism Receptors, Estrogen - drug effects Receptors, Estrogen - genetics Receptors, Estrogen - metabolism Receptors, Progesterone - drug effects Receptors, Progesterone - genetics Receptors, Progesterone - metabolism Transcription Factors - drug effects Transcription Factors - metabolism Transcription, Genetic Tumor Cells, Cultured Tumors |
| title | Estrogen and aryl hydrocarbon receptor expression and crosstalk in human Ishikawa endometrial cancer cells |
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