Tamoxifen-mediated growth inhibition of human cholangiocarcinoma
Cholangiocarcinoma represents a challenging primary malignancy of the liver with no effective medical therapy and a poor prognosis. We have investigated the role of tamoxifen and estrogen receptors (ERs) in the regulation of growth of human cholangiocarcinoma. Two human cholangiocarcinoma cell lines...
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Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1997-05, Vol.57 (9), p.1743-1749 |
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description | Cholangiocarcinoma represents a challenging primary malignancy of the liver with no effective medical therapy and a poor prognosis. We have investigated the role of tamoxifen and estrogen receptors (ERs) in the regulation of growth of human cholangiocarcinoma. Two human cholangiocarcinoma cell lines, OZ and SK-ChA-1, were grown in the presence of graded concentrations of tamoxifen; the effects on cell growth were determined by cell counting or 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium proliferation assay. The presence of ER protein was tested by indirect immunofluorescence and immunoprecipitation. In addition, cells were grown in estrogen-depleted media supplemented with exogenous 17beta-estradiol. ER mRNA was evaluated by reverse transcription-PCR and Northern blotting. Finally, one cholangiocarcinoma cell line was grown as a xenograft in athymic nude mice; tamoxifen effects on in vivo tumor growth were determined with biweekly caliper measurements. Tamoxifen (5-10 microM) caused dose-dependent in vitro growth inhibition of two human cholangiocarcinoma cell lines. In addition, growth inhibition of one cell line (SK-ChA-1) grown as a xenograft in nude mice by tamoxifen was observed. The presence of ER protein was suggested by 17beta-estradiol stimulation of tumor cell growth in vitro and confirmed by immunoprecipitation. Immunofluorescence microscopy was ineffective at detection of ER protein. Reverse transcription-PCR demonstrated the presence of ER mRNA in both cell lines. Northern blot analysis confirmed the presence of full-length 6.5-kb ER mRNA. No ER deletion mutants were detected. Tamoxifen inhibited the growth of human cholangiocarcinoma in vitro and in vivo. ER protein and mRNA were detected in both cell lines. The mechanism(s) of tamoxifen-mediated growth inhibition is unclear but may occur via ER protein or additional pathways. The ability of tamoxifen to inhibit tumor growth may offer an alternative adjunctive treatment for cholangiocarcinoma. |
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K ; VICKERS, S. M ; YING, W ; PHILLIPS, J. O</creator><creatorcontrib>SAMPSON, L. K ; VICKERS, S. M ; YING, W ; PHILLIPS, J. O</creatorcontrib><description>Cholangiocarcinoma represents a challenging primary malignancy of the liver with no effective medical therapy and a poor prognosis. We have investigated the role of tamoxifen and estrogen receptors (ERs) in the regulation of growth of human cholangiocarcinoma. Two human cholangiocarcinoma cell lines, OZ and SK-ChA-1, were grown in the presence of graded concentrations of tamoxifen; the effects on cell growth were determined by cell counting or 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium proliferation assay. The presence of ER protein was tested by indirect immunofluorescence and immunoprecipitation. In addition, cells were grown in estrogen-depleted media supplemented with exogenous 17beta-estradiol. ER mRNA was evaluated by reverse transcription-PCR and Northern blotting. Finally, one cholangiocarcinoma cell line was grown as a xenograft in athymic nude mice; tamoxifen effects on in vivo tumor growth were determined with biweekly caliper measurements. Tamoxifen (5-10 microM) caused dose-dependent in vitro growth inhibition of two human cholangiocarcinoma cell lines. In addition, growth inhibition of one cell line (SK-ChA-1) grown as a xenograft in nude mice by tamoxifen was observed. The presence of ER protein was suggested by 17beta-estradiol stimulation of tumor cell growth in vitro and confirmed by immunoprecipitation. Immunofluorescence microscopy was ineffective at detection of ER protein. Reverse transcription-PCR demonstrated the presence of ER mRNA in both cell lines. Northern blot analysis confirmed the presence of full-length 6.5-kb ER mRNA. No ER deletion mutants were detected. Tamoxifen inhibited the growth of human cholangiocarcinoma in vitro and in vivo. ER protein and mRNA were detected in both cell lines. The mechanism(s) of tamoxifen-mediated growth inhibition is unclear but may occur via ER protein or additional pathways. The ability of tamoxifen to inhibit tumor growth may offer an alternative adjunctive treatment for cholangiocarcinoma.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 9135018</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; Blotting, Northern ; Cell Division - drug effects ; Chemotherapy ; Cholangiocarcinoma - drug therapy ; Cholangiocarcinoma - pathology ; Female ; Gene Expression Regulation, Neoplastic ; Growth Inhibitors - pharmacology ; Humans ; Liver Neoplasms - drug therapy ; Liver Neoplasms - pathology ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Pharmacology. Drug treatments ; Precipitin Tests ; Receptors, Estrogen - genetics ; Tamoxifen - pharmacology ; Tumor Cells, Cultured</subject><ispartof>Cancer research (Chicago, Ill.), 1997-05, Vol.57 (9), p.1743-1749</ispartof><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2669174$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9135018$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SAMPSON, L. K</creatorcontrib><creatorcontrib>VICKERS, S. M</creatorcontrib><creatorcontrib>YING, W</creatorcontrib><creatorcontrib>PHILLIPS, J. O</creatorcontrib><title>Tamoxifen-mediated growth inhibition of human cholangiocarcinoma</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Cholangiocarcinoma represents a challenging primary malignancy of the liver with no effective medical therapy and a poor prognosis. We have investigated the role of tamoxifen and estrogen receptors (ERs) in the regulation of growth of human cholangiocarcinoma. Two human cholangiocarcinoma cell lines, OZ and SK-ChA-1, were grown in the presence of graded concentrations of tamoxifen; the effects on cell growth were determined by cell counting or 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium proliferation assay. The presence of ER protein was tested by indirect immunofluorescence and immunoprecipitation. In addition, cells were grown in estrogen-depleted media supplemented with exogenous 17beta-estradiol. ER mRNA was evaluated by reverse transcription-PCR and Northern blotting. Finally, one cholangiocarcinoma cell line was grown as a xenograft in athymic nude mice; tamoxifen effects on in vivo tumor growth were determined with biweekly caliper measurements. Tamoxifen (5-10 microM) caused dose-dependent in vitro growth inhibition of two human cholangiocarcinoma cell lines. In addition, growth inhibition of one cell line (SK-ChA-1) grown as a xenograft in nude mice by tamoxifen was observed. The presence of ER protein was suggested by 17beta-estradiol stimulation of tumor cell growth in vitro and confirmed by immunoprecipitation. Immunofluorescence microscopy was ineffective at detection of ER protein. Reverse transcription-PCR demonstrated the presence of ER mRNA in both cell lines. Northern blot analysis confirmed the presence of full-length 6.5-kb ER mRNA. No ER deletion mutants were detected. Tamoxifen inhibited the growth of human cholangiocarcinoma in vitro and in vivo. ER protein and mRNA were detected in both cell lines. The mechanism(s) of tamoxifen-mediated growth inhibition is unclear but may occur via ER protein or additional pathways. The ability of tamoxifen to inhibit tumor growth may offer an alternative adjunctive treatment for cholangiocarcinoma.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>Cell Division - drug effects</subject><subject>Chemotherapy</subject><subject>Cholangiocarcinoma - drug therapy</subject><subject>Cholangiocarcinoma - pathology</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Growth Inhibitors - pharmacology</subject><subject>Humans</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Pharmacology. Drug treatments</subject><subject>Precipitin Tests</subject><subject>Receptors, Estrogen - genetics</subject><subject>Tamoxifen - pharmacology</subject><subject>Tumor Cells, Cultured</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9j0FLxDAUhIMo67r6E4QexFshbZImuSmLrsKCl_VcXpOXbaRN1qZF_fcWLJ6GYYZhvjOyLgRTueRcnJM1pVTlgsvyklyl9DFbUVCxIitdMEELtSYPB-jjt3cY8h6thxFtdhzi19hmPrS-8aOPIYsua6ceQmba2EE4-mhgMD7EHq7JhYMu4c2iG_L-_HTYvuT7t93r9nGft2WlxryypeGUzw8YFoZDhWUlG8GM5aC0FRQcRa0cWF2iBe4YOgvGyUYajUyxDbn_2z0N8XPCNNa9Twa7-Q7GKdVSac3EDL8ht0txamak-jT4HoafekGe87slh2SgcwME49N_rawqXUjOfgHc82FV</recordid><startdate>19970501</startdate><enddate>19970501</enddate><creator>SAMPSON, L. K</creator><creator>VICKERS, S. M</creator><creator>YING, W</creator><creator>PHILLIPS, J. O</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19970501</creationdate><title>Tamoxifen-mediated growth inhibition of human cholangiocarcinoma</title><author>SAMPSON, L. K ; VICKERS, S. M ; YING, W ; PHILLIPS, J. O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h268t-6d2c4040003e1c4a6e267b53cd4a89d50af0e98fad92eda4f3efdacf7b7c9e383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Blotting, Northern</topic><topic>Cell Division - drug effects</topic><topic>Chemotherapy</topic><topic>Cholangiocarcinoma - drug therapy</topic><topic>Cholangiocarcinoma - pathology</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Growth Inhibitors - pharmacology</topic><topic>Humans</topic><topic>Liver Neoplasms - drug therapy</topic><topic>Liver Neoplasms - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Pharmacology. Drug treatments</topic><topic>Precipitin Tests</topic><topic>Receptors, Estrogen - genetics</topic><topic>Tamoxifen - pharmacology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SAMPSON, L. K</creatorcontrib><creatorcontrib>VICKERS, S. M</creatorcontrib><creatorcontrib>YING, W</creatorcontrib><creatorcontrib>PHILLIPS, J. O</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>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SAMPSON, L. K</au><au>VICKERS, S. M</au><au>YING, W</au><au>PHILLIPS, J. O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tamoxifen-mediated growth inhibition of human cholangiocarcinoma</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1997-05-01</date><risdate>1997</risdate><volume>57</volume><issue>9</issue><spage>1743</spage><epage>1749</epage><pages>1743-1749</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Cholangiocarcinoma represents a challenging primary malignancy of the liver with no effective medical therapy and a poor prognosis. We have investigated the role of tamoxifen and estrogen receptors (ERs) in the regulation of growth of human cholangiocarcinoma. Two human cholangiocarcinoma cell lines, OZ and SK-ChA-1, were grown in the presence of graded concentrations of tamoxifen; the effects on cell growth were determined by cell counting or 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium proliferation assay. The presence of ER protein was tested by indirect immunofluorescence and immunoprecipitation. In addition, cells were grown in estrogen-depleted media supplemented with exogenous 17beta-estradiol. ER mRNA was evaluated by reverse transcription-PCR and Northern blotting. Finally, one cholangiocarcinoma cell line was grown as a xenograft in athymic nude mice; tamoxifen effects on in vivo tumor growth were determined with biweekly caliper measurements. Tamoxifen (5-10 microM) caused dose-dependent in vitro growth inhibition of two human cholangiocarcinoma cell lines. In addition, growth inhibition of one cell line (SK-ChA-1) grown as a xenograft in nude mice by tamoxifen was observed. The presence of ER protein was suggested by 17beta-estradiol stimulation of tumor cell growth in vitro and confirmed by immunoprecipitation. Immunofluorescence microscopy was ineffective at detection of ER protein. Reverse transcription-PCR demonstrated the presence of ER mRNA in both cell lines. Northern blot analysis confirmed the presence of full-length 6.5-kb ER mRNA. No ER deletion mutants were detected. Tamoxifen inhibited the growth of human cholangiocarcinoma in vitro and in vivo. ER protein and mRNA were detected in both cell lines. The mechanism(s) of tamoxifen-mediated growth inhibition is unclear but may occur via ER protein or additional pathways. The ability of tamoxifen to inhibit tumor growth may offer an alternative adjunctive treatment for cholangiocarcinoma.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>9135018</pmid><tpages>7</tpages></addata></record> |
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subjects | Animals Antineoplastic agents Biological and medical sciences Blotting, Northern Cell Division - drug effects Chemotherapy Cholangiocarcinoma - drug therapy Cholangiocarcinoma - pathology Female Gene Expression Regulation, Neoplastic Growth Inhibitors - pharmacology Humans Liver Neoplasms - drug therapy Liver Neoplasms - pathology Medical sciences Mice Mice, Inbred BALB C Mice, Nude Pharmacology. Drug treatments Precipitin Tests Receptors, Estrogen - genetics Tamoxifen - pharmacology Tumor Cells, Cultured |
title | Tamoxifen-mediated growth inhibition of human cholangiocarcinoma |
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