Regulation of NF-κB activity by IκB-related proteins in adenocarcinoma cells
Constitutive NF-κB activity varies widely among cancer cell lines. In this report, we studied the expression and the role of different IκB inhibitors in adenocarcinoma cell lines. High constitutive NF-κB activity and low IκB-α expression was found in a number of these cell lines. Moreover, some of t...
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Veröffentlicht in: | Oncogene 1999-04, Vol.18 (16), p.2567-2577 |
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creator | DEJARDIN, E DEREGOWSKI, V CHAPELIER, M JACOBS, N GIELEN, J MERVILLE, M.-P BOURS, V |
description | Constitutive NF-κB activity varies widely among cancer cell lines. In this report, we studied the expression and the role of different IκB inhibitors in adenocarcinoma cell lines. High constitutive NF-κB activity and low IκB-α expression was found in a number of these cell lines. Moreover, some of these cells showed a high p100 expression, responsible for the cytoplasmic sequestration of most of p65 complexes. Treatment of these cells with TNF-α or other NF-κB activating agents induced only weakly nuclear NF-κB activity without significant p100 processing and led to a very weak transcription of NF-κB-dependent reporter gene. Induction of NF-κB activity can be restored by expression of the Tax protein or by treatment with antisense p100 oligonucleotides. In MCF7 A/Z cells stably transfected with a p100 expression vector, p65 complexes were sequestered in the cytoplasm by p100. These cells showed a reduced nuclear NF-κB induction and NF-κB-dependent gene transcription following TNF-α stimulation. As a consequence of a competition between IκB-α and p100, cells expressing high levels of p100 respond poorly to NF-κB activating stimuli as TNF-α. |
doi_str_mv | 10.1038/sj.onc.1202599 |
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In this report, we studied the expression and the role of different IκB inhibitors in adenocarcinoma cell lines. High constitutive NF-κB activity and low IκB-α expression was found in a number of these cell lines. Moreover, some of these cells showed a high p100 expression, responsible for the cytoplasmic sequestration of most of p65 complexes. Treatment of these cells with TNF-α or other NF-κB activating agents induced only weakly nuclear NF-κB activity without significant p100 processing and led to a very weak transcription of NF-κB-dependent reporter gene. Induction of NF-κB activity can be restored by expression of the Tax protein or by treatment with antisense p100 oligonucleotides. In MCF7 A/Z cells stably transfected with a p100 expression vector, p65 complexes were sequestered in the cytoplasm by p100. These cells showed a reduced nuclear NF-κB induction and NF-κB-dependent gene transcription following TNF-α stimulation. As a consequence of a competition between IκB-α and p100, cells expressing high levels of p100 respond poorly to NF-κB activating stimuli as TNF-α.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1202599</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Adenocarcinoma ; Antisense oligonucleotides ; Biological and medical sciences ; Cancer ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cytoplasm ; Fundamental and applied biological sciences. Psychology ; Molecular and cellular biology ; NF-κB protein ; Oligonucleotides ; Reporter gene ; Tax protein ; Transcription ; Tumor cell lines ; Tumor necrosis factor-α</subject><ispartof>Oncogene, 1999-04, Vol.18 (16), p.2567-2577</ispartof><rights>1999 INIST-CNRS</rights><rights>Macmillan Publishers Limited 1999.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c325t-1db5f7b81792ab0abd323bce0c8f6fc27903b0f7a5768b7e9d38b53f644215cd3</citedby><cites>FETCH-LOGICAL-c325t-1db5f7b81792ab0abd323bce0c8f6fc27903b0f7a5768b7e9d38b53f644215cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1791229$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>DEJARDIN, E</creatorcontrib><creatorcontrib>DEREGOWSKI, V</creatorcontrib><creatorcontrib>CHAPELIER, M</creatorcontrib><creatorcontrib>JACOBS, N</creatorcontrib><creatorcontrib>GIELEN, J</creatorcontrib><creatorcontrib>MERVILLE, M.-P</creatorcontrib><creatorcontrib>BOURS, V</creatorcontrib><title>Regulation of NF-κB activity by IκB-related proteins in adenocarcinoma cells</title><title>Oncogene</title><description>Constitutive NF-κB activity varies widely among cancer cell lines. In this report, we studied the expression and the role of different IκB inhibitors in adenocarcinoma cell lines. High constitutive NF-κB activity and low IκB-α expression was found in a number of these cell lines. Moreover, some of these cells showed a high p100 expression, responsible for the cytoplasmic sequestration of most of p65 complexes. Treatment of these cells with TNF-α or other NF-κB activating agents induced only weakly nuclear NF-κB activity without significant p100 processing and led to a very weak transcription of NF-κB-dependent reporter gene. Induction of NF-κB activity can be restored by expression of the Tax protein or by treatment with antisense p100 oligonucleotides. In MCF7 A/Z cells stably transfected with a p100 expression vector, p65 complexes were sequestered in the cytoplasm by p100. These cells showed a reduced nuclear NF-κB induction and NF-κB-dependent gene transcription following TNF-α stimulation. As a consequence of a competition between IκB-α and p100, cells expressing high levels of p100 respond poorly to NF-κB activating stimuli as TNF-α.</description><subject>Adenocarcinoma</subject><subject>Antisense oligonucleotides</subject><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cytoplasm</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Molecular and cellular biology</subject><subject>NF-κB protein</subject><subject>Oligonucleotides</subject><subject>Reporter gene</subject><subject>Tax protein</subject><subject>Transcription</subject><subject>Tumor cell lines</subject><subject>Tumor necrosis factor-α</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNpdkF1LBCEUhiUK2j5uuxaK7mbT4ziOlxV9QRREXYs6Gi6zWjob7F_rR_SbMloIujpweN6XhxehI0rmlLD-rCzmKdo5BQJcyi00o63oGs5lu41mRHLSSGCwi_ZKWRBChCQwQw9P7nU16imkiJPHD9fN1-cF1nYKH2FaY7PGd_XRZFcZN-C3nCYXYsEhYj24mKzONsS01Ni6cSwHaMfrsbjDzd1HL9dXz5e3zf3jzd3l-X1jGfCpoYPhXpieCgnaEG0GBsxYR2zvO2-hujFDvNBcdL0RTg6sN5z5rm2BcjuwfXT621uF3leuTGoZyo-Bji6tiqICmCSdrODxP3CRVjlWNwVdS0EIAKjU_JeyOZWSnVdvOSx1XitK1M-4qixUHVdtxq2Bk02tLlaPPutoQ_lLCUkBJPsGSQt7XQ</recordid><startdate>19990422</startdate><enddate>19990422</enddate><creator>DEJARDIN, E</creator><creator>DEREGOWSKI, V</creator><creator>CHAPELIER, M</creator><creator>JACOBS, N</creator><creator>GIELEN, J</creator><creator>MERVILLE, M.-P</creator><creator>BOURS, V</creator><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>19990422</creationdate><title>Regulation of NF-κB activity by IκB-related proteins in adenocarcinoma cells</title><author>DEJARDIN, E ; DEREGOWSKI, V ; CHAPELIER, M ; JACOBS, N ; GIELEN, J ; MERVILLE, M.-P ; BOURS, V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c325t-1db5f7b81792ab0abd323bce0c8f6fc27903b0f7a5768b7e9d38b53f644215cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adenocarcinoma</topic><topic>Antisense oligonucleotides</topic><topic>Biological and medical sciences</topic><topic>Cancer</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cytoplasm</topic><topic>Fundamental and applied biological sciences. 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In this report, we studied the expression and the role of different IκB inhibitors in adenocarcinoma cell lines. High constitutive NF-κB activity and low IκB-α expression was found in a number of these cell lines. Moreover, some of these cells showed a high p100 expression, responsible for the cytoplasmic sequestration of most of p65 complexes. Treatment of these cells with TNF-α or other NF-κB activating agents induced only weakly nuclear NF-κB activity without significant p100 processing and led to a very weak transcription of NF-κB-dependent reporter gene. Induction of NF-κB activity can be restored by expression of the Tax protein or by treatment with antisense p100 oligonucleotides. In MCF7 A/Z cells stably transfected with a p100 expression vector, p65 complexes were sequestered in the cytoplasm by p100. These cells showed a reduced nuclear NF-κB induction and NF-κB-dependent gene transcription following TNF-α stimulation. 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subjects | Adenocarcinoma Antisense oligonucleotides Biological and medical sciences Cancer Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cytoplasm Fundamental and applied biological sciences. Psychology Molecular and cellular biology NF-κB protein Oligonucleotides Reporter gene Tax protein Transcription Tumor cell lines Tumor necrosis factor-α |
title | Regulation of NF-κB activity by IκB-related proteins in adenocarcinoma cells |
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