Novel detection and differential utilization of a c-myc transcriptional block in colon cancer chemoprevention
Mutations in the adenomatous polyposis coli (APC) gene, which initiate almost all human colon cancers, directly target the proto-oncogene, c-myc, by elevating beta-catenin/T-cell factor (TCF) signaling. We have shown that agents ascribed chemopreventive activity for colon cancer in fact also stimula...
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Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2002-11, Vol.62 (21), p.6006-6010 |
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creator | WILSON, Andrew J VELCICH, Anna ARANGO, Diego KURLAND, Amy R SHENOY, Shailesh M PEZO, Rossanna C LEVSKY, Jeffrey M SINGER, Robert H AUGENLICHT, Leonard H |
description | Mutations in the adenomatous polyposis coli (APC) gene, which initiate almost all human colon cancers, directly target the proto-oncogene, c-myc, by elevating beta-catenin/T-cell factor (TCF) signaling. We have shown that agents ascribed chemopreventive activity for colon cancer in fact also stimulate beta-catenin/TCF activity in vitro. Their effects on c-myc transcription were assayed using a novel variant of fluorescence in situ hybridization that detects c-myc transcription sites in intact nuclei. Increased transcriptional initiation of c-myc induced by the short-chain fatty acid, butyrate, consistent with elevated beta-catenin/TCF activity, was efficiently abrogated by a block to transcriptional elongation, resulting in decreased c-myc expression. 1alpha,25-Dihydroxyvitamin D(3) also induced transcriptional blockage. In contrast, the nonsteroidal anti-inflammatory drug, sulindac, increased c-myc expression, an effect attributable at least in part to its failure to induce transcriptional blockage. We have described a novel approach for evaluating the effects of chemopreventive agents on the expression of a gene critical in colonic tumorigenesis. |
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We have shown that agents ascribed chemopreventive activity for colon cancer in fact also stimulate beta-catenin/TCF activity in vitro. Their effects on c-myc transcription were assayed using a novel variant of fluorescence in situ hybridization that detects c-myc transcription sites in intact nuclei. Increased transcriptional initiation of c-myc induced by the short-chain fatty acid, butyrate, consistent with elevated beta-catenin/TCF activity, was efficiently abrogated by a block to transcriptional elongation, resulting in decreased c-myc expression. 1alpha,25-Dihydroxyvitamin D(3) also induced transcriptional blockage. In contrast, the nonsteroidal anti-inflammatory drug, sulindac, increased c-myc expression, an effect attributable at least in part to its failure to induce transcriptional blockage. We have described a novel approach for evaluating the effects of chemopreventive agents on the expression of a gene critical in colonic tumorigenesis.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 12414619</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Anticarcinogenic Agents - pharmacology ; Biological and medical sciences ; Butyrates - pharmacology ; Carcinogenesis, carcinogens and anticarcinogens ; Chemical agents ; Colonic Neoplasms - genetics ; Colonic Neoplasms - prevention & control ; Dihydroxycholecalciferols - pharmacology ; DNA Probes ; Drug Interactions ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Expression Regulation, Neoplastic - genetics ; Gene Silencing - drug effects ; Genes, myc - drug effects ; Genes, myc - genetics ; Genetic Predisposition to Disease ; Humans ; Medical sciences ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Sulindac - pharmacology ; Transcription, Genetic - drug effects ; Transcription, Genetic - genetics ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 2002-11, Vol.62 (21), p.6006-6010</ispartof><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13998281$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12414619$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WILSON, Andrew J</creatorcontrib><creatorcontrib>VELCICH, Anna</creatorcontrib><creatorcontrib>ARANGO, Diego</creatorcontrib><creatorcontrib>KURLAND, Amy R</creatorcontrib><creatorcontrib>SHENOY, Shailesh M</creatorcontrib><creatorcontrib>PEZO, Rossanna C</creatorcontrib><creatorcontrib>LEVSKY, Jeffrey M</creatorcontrib><creatorcontrib>SINGER, Robert H</creatorcontrib><creatorcontrib>AUGENLICHT, Leonard H</creatorcontrib><title>Novel detection and differential utilization of a c-myc transcriptional block in colon cancer chemoprevention</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Mutations in the adenomatous polyposis coli (APC) gene, which initiate almost all human colon cancers, directly target the proto-oncogene, c-myc, by elevating beta-catenin/T-cell factor (TCF) signaling. We have shown that agents ascribed chemopreventive activity for colon cancer in fact also stimulate beta-catenin/TCF activity in vitro. Their effects on c-myc transcription were assayed using a novel variant of fluorescence in situ hybridization that detects c-myc transcription sites in intact nuclei. Increased transcriptional initiation of c-myc induced by the short-chain fatty acid, butyrate, consistent with elevated beta-catenin/TCF activity, was efficiently abrogated by a block to transcriptional elongation, resulting in decreased c-myc expression. 1alpha,25-Dihydroxyvitamin D(3) also induced transcriptional blockage. In contrast, the nonsteroidal anti-inflammatory drug, sulindac, increased c-myc expression, an effect attributable at least in part to its failure to induce transcriptional blockage. We have described a novel approach for evaluating the effects of chemopreventive agents on the expression of a gene critical in colonic tumorigenesis.</description><subject>Anticarcinogenic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Butyrates - pharmacology</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Chemical agents</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - prevention & control</subject><subject>Dihydroxycholecalciferols - pharmacology</subject><subject>DNA Probes</subject><subject>Drug Interactions</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene Silencing - drug effects</subject><subject>Genes, myc - drug effects</subject><subject>Genes, myc - genetics</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Sulindac - pharmacology</subject><subject>Transcription, Genetic - drug effects</subject><subject>Transcription, Genetic - genetics</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFj01LAzEYhIMotlb_guTicSHZJLvJUYofhaIXPZfsm4RGs8mS3RbqrzfViqdhmIdh5gzNqWCyajkX52hOCJGV4G09Q1fj-FGsoERcohmtOeUNVXPUv6S9DdjYycLkU8Q6Gmy8czbbOHkd8G7ywX_pnzA5rDFU_QHwlHUcIfvhGBSsCwk-sY8YUigk6Ag2Y9jaPg3Z7o9lKV6jC6fDaG9OukDvjw9vy-dq_fq0Wt6vq23d0qmyxjHVUOFc1wAXLTBnW2JUJ1TdaC5dTQjnppVE6k4CADPUsSLSdKpMZwt0-9s77Lrems2Qfa_zYfP3uwB3J0CPoIMrZ8CP_xxTStaSsm_lwGU-</recordid><startdate>20021101</startdate><enddate>20021101</enddate><creator>WILSON, Andrew J</creator><creator>VELCICH, Anna</creator><creator>ARANGO, Diego</creator><creator>KURLAND, Amy R</creator><creator>SHENOY, Shailesh M</creator><creator>PEZO, Rossanna C</creator><creator>LEVSKY, Jeffrey M</creator><creator>SINGER, Robert H</creator><creator>AUGENLICHT, Leonard H</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></search><sort><creationdate>20021101</creationdate><title>Novel detection and differential utilization of a c-myc transcriptional block in colon cancer chemoprevention</title><author>WILSON, Andrew J ; VELCICH, Anna ; ARANGO, Diego ; KURLAND, Amy R ; SHENOY, Shailesh M ; PEZO, Rossanna C ; LEVSKY, Jeffrey M ; SINGER, Robert H ; AUGENLICHT, Leonard H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h271t-edf39615ffb6c457c3fe70d9b5926a48f20044d7808ab8ccc3d1f3cc38db9ffe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Anticarcinogenic Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Butyrates - pharmacology</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Chemical agents</topic><topic>Colonic Neoplasms - genetics</topic><topic>Colonic Neoplasms - prevention & control</topic><topic>Dihydroxycholecalciferols - pharmacology</topic><topic>DNA Probes</topic><topic>Drug Interactions</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene Silencing - drug effects</topic><topic>Genes, myc - drug effects</topic><topic>Genes, myc - genetics</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Sulindac - pharmacology</topic><topic>Transcription, Genetic - drug effects</topic><topic>Transcription, Genetic - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WILSON, Andrew J</creatorcontrib><creatorcontrib>VELCICH, Anna</creatorcontrib><creatorcontrib>ARANGO, Diego</creatorcontrib><creatorcontrib>KURLAND, Amy R</creatorcontrib><creatorcontrib>SHENOY, Shailesh M</creatorcontrib><creatorcontrib>PEZO, Rossanna C</creatorcontrib><creatorcontrib>LEVSKY, Jeffrey M</creatorcontrib><creatorcontrib>SINGER, Robert H</creatorcontrib><creatorcontrib>AUGENLICHT, Leonard H</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WILSON, Andrew J</au><au>VELCICH, Anna</au><au>ARANGO, Diego</au><au>KURLAND, Amy R</au><au>SHENOY, Shailesh M</au><au>PEZO, Rossanna C</au><au>LEVSKY, Jeffrey M</au><au>SINGER, Robert H</au><au>AUGENLICHT, Leonard H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Novel detection and differential utilization of a c-myc transcriptional block in colon cancer chemoprevention</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2002-11-01</date><risdate>2002</risdate><volume>62</volume><issue>21</issue><spage>6006</spage><epage>6010</epage><pages>6006-6010</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Mutations in the adenomatous polyposis coli (APC) gene, which initiate almost all human colon cancers, directly target the proto-oncogene, c-myc, by elevating beta-catenin/T-cell factor (TCF) signaling. We have shown that agents ascribed chemopreventive activity for colon cancer in fact also stimulate beta-catenin/TCF activity in vitro. Their effects on c-myc transcription were assayed using a novel variant of fluorescence in situ hybridization that detects c-myc transcription sites in intact nuclei. Increased transcriptional initiation of c-myc induced by the short-chain fatty acid, butyrate, consistent with elevated beta-catenin/TCF activity, was efficiently abrogated by a block to transcriptional elongation, resulting in decreased c-myc expression. 1alpha,25-Dihydroxyvitamin D(3) also induced transcriptional blockage. In contrast, the nonsteroidal anti-inflammatory drug, sulindac, increased c-myc expression, an effect attributable at least in part to its failure to induce transcriptional blockage. We have described a novel approach for evaluating the effects of chemopreventive agents on the expression of a gene critical in colonic tumorigenesis.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>12414619</pmid><tpages>5</tpages></addata></record> |
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subjects | Anticarcinogenic Agents - pharmacology Biological and medical sciences Butyrates - pharmacology Carcinogenesis, carcinogens and anticarcinogens Chemical agents Colonic Neoplasms - genetics Colonic Neoplasms - prevention & control Dihydroxycholecalciferols - pharmacology DNA Probes Drug Interactions Gene Expression Regulation, Neoplastic - drug effects Gene Expression Regulation, Neoplastic - genetics Gene Silencing - drug effects Genes, myc - drug effects Genes, myc - genetics Genetic Predisposition to Disease Humans Medical sciences RNA, Messenger - biosynthesis RNA, Messenger - genetics RNA, Messenger - metabolism Sulindac - pharmacology Transcription, Genetic - drug effects Transcription, Genetic - genetics Tumors |
title | Novel detection and differential utilization of a c-myc transcriptional block in colon cancer chemoprevention |
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