Characterization of transforming growth factor-β-resistant subclones isolated from a transforming growth factor-β-sensitive human colon carcinoma cell line
Previous work indicated that transforming growth factor-beta (TGF-beta) elicits proliferation-inhibitory effects in the human colon carcinoma cell line MOSER. This paper describes the isolation and characterization of spontaneously arising subclones from this TGF-beta-sensitive parental line which w...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1988-12, Vol.48 (24), p.7120-7125 |
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| container_title | Cancer research (Chicago, Ill.) |
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| creator | MULDER, K. M RAMEY, M. K HOOSEIN, N. M LEVINE, A. E HINSHAW, X. H BRATTAIN, D. E BRATTAIN, M. G |
| description | Previous work indicated that transforming growth factor-beta (TGF-beta) elicits proliferation-inhibitory effects in the human colon carcinoma cell line MOSER. This paper describes the isolation and characterization of spontaneously arising subclones from this TGF-beta-sensitive parental line which were relatively refractory to the inhibitory effects of TGF-beta. While the parental cell line responded to TGF-beta with an inhibition of cellular proliferation in monolayer culture and in soft agarose, an increase in extracellular fibronectin, and a down-regulation of c-myc protooncogene expression, these responses were absent or attenuated in the sublines. However, the resistant clones retained the ability to specifically bind TGF-beta. N,N-Dimethylformamide and retinoic acid, two other agents associated with induction of a partial differentiation-like response in the MOSER parental cells (similar to that elicited by TGF-beta), inhibited the monolayer proliferation of both the parental cells and the TGF-beta-resistant sublines. Thus, the refractoriness observed in the isolated clones was relatively specific for TGF-beta. |
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M ; RAMEY, M. K ; HOOSEIN, N. M ; LEVINE, A. E ; HINSHAW, X. H ; BRATTAIN, D. E ; BRATTAIN, M. G</creator><creatorcontrib>MULDER, K. M ; RAMEY, M. K ; HOOSEIN, N. M ; LEVINE, A. E ; HINSHAW, X. H ; BRATTAIN, D. E ; BRATTAIN, M. G</creatorcontrib><description>Previous work indicated that transforming growth factor-beta (TGF-beta) elicits proliferation-inhibitory effects in the human colon carcinoma cell line MOSER. This paper describes the isolation and characterization of spontaneously arising subclones from this TGF-beta-sensitive parental line which were relatively refractory to the inhibitory effects of TGF-beta. While the parental cell line responded to TGF-beta with an inhibition of cellular proliferation in monolayer culture and in soft agarose, an increase in extracellular fibronectin, and a down-regulation of c-myc protooncogene expression, these responses were absent or attenuated in the sublines. However, the resistant clones retained the ability to specifically bind TGF-beta. N,N-Dimethylformamide and retinoic acid, two other agents associated with induction of a partial differentiation-like response in the MOSER parental cells (similar to that elicited by TGF-beta), inhibited the monolayer proliferation of both the parental cells and the TGF-beta-resistant sublines. Thus, the refractoriness observed in the isolated clones was relatively specific for TGF-beta.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 3191488</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Biological and medical sciences ; Cell Line ; Clone Cells - drug effects ; Colonic Neoplasms - pathology ; Dimethylformamide - pharmacology ; Drug Resistance ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Medical sciences ; Oncogenes ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Transforming Growth Factors - pharmacology ; Tretinoin - pharmacology ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 1988-12, Vol.48 (24), p.7120-7125</ispartof><rights>1989 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=7189011$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3191488$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MULDER, K. M</creatorcontrib><creatorcontrib>RAMEY, M. K</creatorcontrib><creatorcontrib>HOOSEIN, N. M</creatorcontrib><creatorcontrib>LEVINE, A. E</creatorcontrib><creatorcontrib>HINSHAW, X. H</creatorcontrib><creatorcontrib>BRATTAIN, D. E</creatorcontrib><creatorcontrib>BRATTAIN, M. G</creatorcontrib><title>Characterization of transforming growth factor-β-resistant subclones isolated from a transforming growth factor-β-sensitive human colon carcinoma cell line</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Previous work indicated that transforming growth factor-beta (TGF-beta) elicits proliferation-inhibitory effects in the human colon carcinoma cell line MOSER. This paper describes the isolation and characterization of spontaneously arising subclones from this TGF-beta-sensitive parental line which were relatively refractory to the inhibitory effects of TGF-beta. While the parental cell line responded to TGF-beta with an inhibition of cellular proliferation in monolayer culture and in soft agarose, an increase in extracellular fibronectin, and a down-regulation of c-myc protooncogene expression, these responses were absent or attenuated in the sublines. However, the resistant clones retained the ability to specifically bind TGF-beta. N,N-Dimethylformamide and retinoic acid, two other agents associated with induction of a partial differentiation-like response in the MOSER parental cells (similar to that elicited by TGF-beta), inhibited the monolayer proliferation of both the parental cells and the TGF-beta-resistant sublines. Thus, the refractoriness observed in the isolated clones was relatively specific for TGF-beta.</description><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Clone Cells - drug effects</subject><subject>Colonic Neoplasms - pathology</subject><subject>Dimethylformamide - pharmacology</subject><subject>Drug Resistance</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Oncogenes</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Transforming Growth Factors - pharmacology</subject><subject>Tretinoin - pharmacology</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1KxDAUhYMo4zj6CEIW4q6Q3zZdyuAfDLjRdblNk5lIm4xJqui7-BI-iM9kBwe3ri6H8_FxOQdoTiVXRSWEPERzQogqpKjYMTpJ6XmKkhI5QzNOayqUmqPP5QYi6Gyi-4DsgsfB4hzBJxvi4Pwar2N4yxtsJyjE4vuriCa5lMFnnMZW98GbhF0KPWTTYRvDgOEfQzI-uexeDd6MA3isw2TBGqJ2PgyAtel73DtvTtGRhT6Zs_1doKeb68flXbF6uL1fXq2KLeMyFyCs5JUthamJlkSUxKgOOs5qWVa2bm1ZtprWRFrB6A5kuhNVqxWztGNlyRfo8te7jeFlNCk3g0u7L8CbMKamUpIzwdkEnu_BsR1M12yjGyC-N_s9p_5i30PS0NtpBu3SH1ZRVRNK-Q_IrIUK</recordid><startdate>19881215</startdate><enddate>19881215</enddate><creator>MULDER, K. M</creator><creator>RAMEY, M. K</creator><creator>HOOSEIN, N. M</creator><creator>LEVINE, A. E</creator><creator>HINSHAW, X. H</creator><creator>BRATTAIN, D. E</creator><creator>BRATTAIN, M. G</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>19881215</creationdate><title>Characterization of transforming growth factor-β-resistant subclones isolated from a transforming growth factor-β-sensitive human colon carcinoma cell line</title><author>MULDER, K. M ; RAMEY, M. K ; HOOSEIN, N. M ; LEVINE, A. E ; HINSHAW, X. H ; BRATTAIN, D. E ; BRATTAIN, M. G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p235t-a4f537f64e90c50460e8dad329567f9bf66bc1905f42137f62cd47bc82f1d2663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Clone Cells - drug effects</topic><topic>Colonic Neoplasms - pathology</topic><topic>Dimethylformamide - pharmacology</topic><topic>Drug Resistance</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Oncogenes</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Transforming Growth Factors - pharmacology</topic><topic>Tretinoin - pharmacology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MULDER, K. M</creatorcontrib><creatorcontrib>RAMEY, M. K</creatorcontrib><creatorcontrib>HOOSEIN, N. M</creatorcontrib><creatorcontrib>LEVINE, A. E</creatorcontrib><creatorcontrib>HINSHAW, X. H</creatorcontrib><creatorcontrib>BRATTAIN, D. E</creatorcontrib><creatorcontrib>BRATTAIN, M. G</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>MULDER, K. M</au><au>RAMEY, M. K</au><au>HOOSEIN, N. M</au><au>LEVINE, A. E</au><au>HINSHAW, X. H</au><au>BRATTAIN, D. E</au><au>BRATTAIN, M. G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization of transforming growth factor-β-resistant subclones isolated from a transforming growth factor-β-sensitive human colon carcinoma cell line</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1988-12-15</date><risdate>1988</risdate><volume>48</volume><issue>24</issue><spage>7120</spage><epage>7125</epage><pages>7120-7125</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Previous work indicated that transforming growth factor-beta (TGF-beta) elicits proliferation-inhibitory effects in the human colon carcinoma cell line MOSER. This paper describes the isolation and characterization of spontaneously arising subclones from this TGF-beta-sensitive parental line which were relatively refractory to the inhibitory effects of TGF-beta. While the parental cell line responded to TGF-beta with an inhibition of cellular proliferation in monolayer culture and in soft agarose, an increase in extracellular fibronectin, and a down-regulation of c-myc protooncogene expression, these responses were absent or attenuated in the sublines. However, the resistant clones retained the ability to specifically bind TGF-beta. N,N-Dimethylformamide and retinoic acid, two other agents associated with induction of a partial differentiation-like response in the MOSER parental cells (similar to that elicited by TGF-beta), inhibited the monolayer proliferation of both the parental cells and the TGF-beta-resistant sublines. Thus, the refractoriness observed in the isolated clones was relatively specific for TGF-beta.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>3191488</pmid><tpages>6</tpages></addata></record> |
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| identifier | ISSN: 0008-5472 |
| ispartof | Cancer research (Chicago, Ill.), 1988-12, Vol.48 (24), p.7120-7125 |
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| language | eng |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Biological and medical sciences Cell Line Clone Cells - drug effects Colonic Neoplasms - pathology Dimethylformamide - pharmacology Drug Resistance Gastroenterology. Liver. Pancreas. Abdomen Humans Medical sciences Oncogenes Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Transforming Growth Factors - pharmacology Tretinoin - pharmacology Tumors |
| title | Characterization of transforming growth factor-β-resistant subclones isolated from a transforming growth factor-β-sensitive human colon carcinoma cell line |
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