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De novo Expression of the Muc2 Gene in Pancreas Carcinoma Cells Is Triggered by Promoter Demethylation
It has been established that mucin-producing variants of different subtypes of pancreatic carcinomas, including the intraductal papillary and ductal mucinous tumors, have usually a more favorable prognosis. Intraductal papillary and ductal mucinous tumors have also been shown to ectopically express...
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Published in: | Tumor biology 2002-01, Vol.23 (1), p.54-60 |
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creator | Siedow, A. Szyf, M. Gratchev, A. Kobalz, U. Hanski, M.-L. Bumke-Vogt, C. Foss, H.D. Riecken, E.O. Hanski, C. |
description | It has been established that mucin-producing variants of different subtypes of pancreatic carcinomas, including the intraductal papillary and ductal mucinous tumors, have usually a more favorable prognosis. Intraductal papillary and ductal mucinous tumors have also been shown to ectopically express the intestinal mucin gene MUC2. The mechanism of the de novo expression of this gene in tumors may have potential implications for the modulation of its behavior. We studied, therefore, the mechanism of the de novo expression of MUC2 in pancreas carcinoma cells in vitro. The MUC2 gene promoter is methylated in the nonexpressing pancreatic cell line PANC-1 and is not methylated in the expressing cell line BxPC-3. The promoter is silenced by methylation as shown by reporter expression assays. De novo expression of MUC2 in PANC-1 cells is triggered by treating the cells with a pharmacological inhibitor of DNA methylation (5-aza-2’-deoxycytidine). There was no decrease or loss of expression of the methyltransferase DNMT1 in the MUC2-producing cells. These data show that the de novo expression of the MUC2 gene in pancreas carcinoma cells is associated with promoter demethylation. They warrant further investigations on the relationship between MUC2 promoter demethylation in pancreatic cancer and the prognosis of carcinoma patients. |
doi_str_mv | 10.1159/000048689 |
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Intraductal papillary and ductal mucinous tumors have also been shown to ectopically express the intestinal mucin gene MUC2. The mechanism of the de novo expression of this gene in tumors may have potential implications for the modulation of its behavior. We studied, therefore, the mechanism of the de novo expression of MUC2 in pancreas carcinoma cells in vitro. The MUC2 gene promoter is methylated in the nonexpressing pancreatic cell line PANC-1 and is not methylated in the expressing cell line BxPC-3. The promoter is silenced by methylation as shown by reporter expression assays. De novo expression of MUC2 in PANC-1 cells is triggered by treating the cells with a pharmacological inhibitor of DNA methylation (5-aza-2’-deoxycytidine). There was no decrease or loss of expression of the methyltransferase DNMT1 in the MUC2-producing cells. These data show that the de novo expression of the MUC2 gene in pancreas carcinoma cells is associated with promoter demethylation. They warrant further investigations on the relationship between MUC2 promoter demethylation in pancreatic cancer and the prognosis of carcinoma patients.</description><identifier>ISSN: 1010-4283</identifier><identifier>EISSN: 1423-0380</identifier><identifier>DOI: 10.1159/000048689</identifier><identifier>PMID: 11893907</identifier><identifier>CODEN: OBIMD4</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Azacitidine - analogs & derivatives ; Azacitidine - pharmacology ; Biological and medical sciences ; Blotting, Northern ; DNA Methylation ; DNA, Complementary - metabolism ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; Genes, Reporter ; Humans ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Luciferases - metabolism ; Medical sciences ; Mucin-2 ; Mucins - biosynthesis ; Mucins - genetics ; Pancreatic Neoplasms - metabolism ; Plasmids - metabolism ; Promoter Regions, Genetic ; Research Article ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Sulfites - pharmacology ; Transfection ; Tumors</subject><ispartof>Tumor biology, 2002-01, Vol.23 (1), p.54-60</ispartof><rights>2002 S. Karger AG, Basel</rights><rights>2002 INIST-CNRS</rights><rights>Copyright 2002 S. Karger AG, Basel</rights><rights>Copyright (c) 2002 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-f223a67288377d79ed18de23d369b0f2d3c50f5ad6745fd4bb6b6ee097f632a73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/222708478?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,4024,25753,27923,27924,27925,37012,37013,44590</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13595798$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11893907$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Siedow, A.</creatorcontrib><creatorcontrib>Szyf, M.</creatorcontrib><creatorcontrib>Gratchev, A.</creatorcontrib><creatorcontrib>Kobalz, U.</creatorcontrib><creatorcontrib>Hanski, M.-L.</creatorcontrib><creatorcontrib>Bumke-Vogt, C.</creatorcontrib><creatorcontrib>Foss, H.D.</creatorcontrib><creatorcontrib>Riecken, E.O.</creatorcontrib><creatorcontrib>Hanski, C.</creatorcontrib><title>De novo Expression of the Muc2 Gene in Pancreas Carcinoma Cells Is Triggered by Promoter Demethylation</title><title>Tumor biology</title><addtitle>Tumor Biol</addtitle><description>It has been established that mucin-producing variants of different subtypes of pancreatic carcinomas, including the intraductal papillary and ductal mucinous tumors, have usually a more favorable prognosis. Intraductal papillary and ductal mucinous tumors have also been shown to ectopically express the intestinal mucin gene MUC2. The mechanism of the de novo expression of this gene in tumors may have potential implications for the modulation of its behavior. We studied, therefore, the mechanism of the de novo expression of MUC2 in pancreas carcinoma cells in vitro. The MUC2 gene promoter is methylated in the nonexpressing pancreatic cell line PANC-1 and is not methylated in the expressing cell line BxPC-3. The promoter is silenced by methylation as shown by reporter expression assays. De novo expression of MUC2 in PANC-1 cells is triggered by treating the cells with a pharmacological inhibitor of DNA methylation (5-aza-2’-deoxycytidine). There was no decrease or loss of expression of the methyltransferase DNMT1 in the MUC2-producing cells. These data show that the de novo expression of the MUC2 gene in pancreas carcinoma cells is associated with promoter demethylation. They warrant further investigations on the relationship between MUC2 promoter demethylation in pancreatic cancer and the prognosis of carcinoma patients.</description><subject>Azacitidine - analogs & derivatives</subject><subject>Azacitidine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>DNA Methylation</subject><subject>DNA, Complementary - metabolism</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Reporter</subject><subject>Humans</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Luciferases - metabolism</subject><subject>Medical sciences</subject><subject>Mucin-2</subject><subject>Mucins - biosynthesis</subject><subject>Mucins - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Plasmids - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Research Article</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Sulfites - pharmacology</subject><subject>Transfection</subject><subject>Tumors</subject><issn>1010-4283</issn><issn>1423-0380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNqF0c1LHDEYB-AgFbXWg-dCCQULHqbN1-TjWFdrF5R6WM9DZvJGx85M1mRG3P--aXdxQQrmkhwefnk_EDqm5CulpflG8hFaarODDqhgvCBck3f5TSgpBNN8H71P6YGQjI3cQ_uUasMNUQfInwMewlPAF8_LCCm1YcDB4_Ee8PXUMHwJA-B2wDd2aCLYhGc2Nu0Qeotn0HUJzxNexPbuDiI4XK_wTQx9GCHic-hhvF91dsyZH9Cut12Co819iG5_XCxmP4urX5fz2ferohGajYVnjFupmNZcKacMOKodMO64NDXxzPGmJL60TipReifqWtYSgBjlJWdW8UP0ZZ27jOFxgjRWfZuaXKgdIEypUrQkRjLxJqRayJIwmuHnV_AhTHHITVSMMUW0UDqj0zVqYkgpgq-Wse1tXFWUVH9XVL2sKNtPm8Cp7sFt5WYnGZxsgE2N7XzMo2_T1vHSlMrobWW_bczjfwGLs_m_n6ql8xl9_C9a1_IHLqCrOA</recordid><startdate>200201</startdate><enddate>200201</enddate><creator>Siedow, A.</creator><creator>Szyf, M.</creator><creator>Gratchev, A.</creator><creator>Kobalz, U.</creator><creator>Hanski, M.-L.</creator><creator>Bumke-Vogt, C.</creator><creator>Foss, H.D.</creator><creator>Riecken, E.O.</creator><creator>Hanski, C.</creator><general>Karger</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>200201</creationdate><title>De novo Expression of the Muc2 Gene in Pancreas Carcinoma Cells Is Triggered by Promoter Demethylation</title><author>Siedow, A. ; Szyf, M. ; Gratchev, A. ; Kobalz, U. ; Hanski, M.-L. ; Bumke-Vogt, C. ; Foss, H.D. ; Riecken, E.O. ; Hanski, C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-f223a67288377d79ed18de23d369b0f2d3c50f5ad6745fd4bb6b6ee097f632a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Azacitidine - analogs & derivatives</topic><topic>Azacitidine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blotting, Northern</topic><topic>DNA Methylation</topic><topic>DNA, Complementary - metabolism</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Reporter</topic><topic>Humans</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Luciferases - metabolism</topic><topic>Medical sciences</topic><topic>Mucin-2</topic><topic>Mucins - biosynthesis</topic><topic>Mucins - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Plasmids - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Research Article</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Sulfites - pharmacology</topic><topic>Transfection</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Siedow, A.</creatorcontrib><creatorcontrib>Szyf, M.</creatorcontrib><creatorcontrib>Gratchev, A.</creatorcontrib><creatorcontrib>Kobalz, U.</creatorcontrib><creatorcontrib>Hanski, M.-L.</creatorcontrib><creatorcontrib>Bumke-Vogt, C.</creatorcontrib><creatorcontrib>Foss, H.D.</creatorcontrib><creatorcontrib>Riecken, E.O.</creatorcontrib><creatorcontrib>Hanski, C.</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>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (ProQuest Medical & Health Databases)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest research library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Tumor biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Siedow, A.</au><au>Szyf, M.</au><au>Gratchev, A.</au><au>Kobalz, U.</au><au>Hanski, M.-L.</au><au>Bumke-Vogt, C.</au><au>Foss, H.D.</au><au>Riecken, E.O.</au><au>Hanski, C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>De novo Expression of the Muc2 Gene in Pancreas Carcinoma Cells Is Triggered by Promoter Demethylation</atitle><jtitle>Tumor biology</jtitle><addtitle>Tumor Biol</addtitle><date>2002-01</date><risdate>2002</risdate><volume>23</volume><issue>1</issue><spage>54</spage><epage>60</epage><pages>54-60</pages><issn>1010-4283</issn><eissn>1423-0380</eissn><coden>OBIMD4</coden><abstract>It has been established that mucin-producing variants of different subtypes of pancreatic carcinomas, including the intraductal papillary and ductal mucinous tumors, have usually a more favorable prognosis. Intraductal papillary and ductal mucinous tumors have also been shown to ectopically express the intestinal mucin gene MUC2. The mechanism of the de novo expression of this gene in tumors may have potential implications for the modulation of its behavior. We studied, therefore, the mechanism of the de novo expression of MUC2 in pancreas carcinoma cells in vitro. The MUC2 gene promoter is methylated in the nonexpressing pancreatic cell line PANC-1 and is not methylated in the expressing cell line BxPC-3. The promoter is silenced by methylation as shown by reporter expression assays. De novo expression of MUC2 in PANC-1 cells is triggered by treating the cells with a pharmacological inhibitor of DNA methylation (5-aza-2’-deoxycytidine). There was no decrease or loss of expression of the methyltransferase DNMT1 in the MUC2-producing cells. These data show that the de novo expression of the MUC2 gene in pancreas carcinoma cells is associated with promoter demethylation. They warrant further investigations on the relationship between MUC2 promoter demethylation in pancreatic cancer and the prognosis of carcinoma patients.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>11893907</pmid><doi>10.1159/000048689</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Azacitidine - analogs & derivatives Azacitidine - pharmacology Biological and medical sciences Blotting, Northern DNA Methylation DNA, Complementary - metabolism Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic Genes, Reporter Humans Liver. Biliary tract. Portal circulation. Exocrine pancreas Luciferases - metabolism Medical sciences Mucin-2 Mucins - biosynthesis Mucins - genetics Pancreatic Neoplasms - metabolism Plasmids - metabolism Promoter Regions, Genetic Research Article Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Sulfites - pharmacology Transfection Tumors |
title | De novo Expression of the Muc2 Gene in Pancreas Carcinoma Cells Is Triggered by Promoter Demethylation |
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