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...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Cancer research (Chicago, Ill.) Ill.), 1997-05, Vol.57 (9), p.1743-1749
Hauptverfasser: SAMPSON, L. K, VICKERS, S. M, YING, W, PHILLIPS, J. O
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 1749
container_issue 9
container_start_page 1743
container_title Cancer research (Chicago, Ill.)
container_volume 57
creator SAMPSON, L. K
VICKERS, S. M
YING, W
PHILLIPS, J. O
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.
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_78993515</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>78993515</sourcerecordid><originalsourceid>FETCH-LOGICAL-h268t-6d2c4040003e1c4a6e267b53cd4a89d50af0e98fad92eda4f3efdacf7b7c9e383</originalsourceid><addsrcrecordid>eNo9j0FLxDAUhIMo67r6E4QexFshbZImuSmLrsKCl_VcXpOXbaRN1qZF_fcWLJ6GYYZhvjOyLgRTueRcnJM1pVTlgsvyklyl9DFbUVCxIitdMEELtSYPB-jjt3cY8h6thxFtdhzi19hmPrS-8aOPIYsua6ceQmba2EE4-mhgMD7EHq7JhYMu4c2iG_L-_HTYvuT7t93r9nGft2WlxryypeGUzw8YFoZDhWUlG8GM5aC0FRQcRa0cWF2iBe4YOgvGyUYajUyxDbn_2z0N8XPCNNa9Twa7-Q7GKdVSac3EDL8ht0txamak-jT4HoafekGe87slh2SgcwME49N_rawqXUjOfgHc82FV</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>78993515</pqid></control><display><type>article</type><title>Tamoxifen-mediated growth inhibition of human cholangiocarcinoma</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>EZB Electronic Journals Library</source><creator>SAMPSON, L. 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&amp;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>
fulltext fulltext
identifier ISSN: 0008-5472
ispartof Cancer research (Chicago, Ill.), 1997-05, Vol.57 (9), p.1743-1749
issn 0008-5472
1538-7445
language eng
recordid cdi_proquest_miscellaneous_78993515
source MEDLINE; American Association for Cancer Research; EZB Electronic Journals Library
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
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T16%3A02%3A31IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Tamoxifen-mediated%20growth%20inhibition%20of%20human%20cholangiocarcinoma&rft.jtitle=Cancer%20research%20(Chicago,%20Ill.)&rft.au=SAMPSON,%20L.%20K&rft.date=1997-05-01&rft.volume=57&rft.issue=9&rft.spage=1743&rft.epage=1749&rft.pages=1743-1749&rft.issn=0008-5472&rft.eissn=1538-7445&rft.coden=CNREA8&rft_id=info:doi/&rft_dat=%3Cproquest_pubme%3E78993515%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=78993515&rft_id=info:pmid/9135018&rfr_iscdi=true