The E-cadherin −347G→GA promoter polymorphism and its effect on transcriptional regulation
E-cadherin plays a critical role in epithelial cell–cell adhesion and maintenance of tissue architecture. Loss of E-cadherin expression in humans has been associated with cancer, and a number of cancer-related mutations have been identified. Here, we sought to investigate whether the −347G→GA single...
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| Veröffentlicht in: | Carcinogenesis (New York) 2004-06, Vol.25 (6), p.895-899 |
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| creator | Shin, Yong Kim, Il-Jin Kang, Hio Chung Park, Jae-Hyun Park, Hye-Rin Park, Hye-Won Park, Mi Ae Lee, Jong Soo Yoon, Kyong-Ah Ku, Ja-Lok Park, Jae-Gahb |
| description | E-cadherin plays a critical role in epithelial cell–cell adhesion and maintenance of tissue architecture. Loss of E-cadherin expression in humans has been associated with cancer, and a number of cancer-related mutations have been identified. Here, we sought to investigate whether the −347G→GA single nucleotide polymorphism affects the transcriptional activity of the E-cadherin gene. First, we measured the promoter activity of the −347G→GA polymorphism using a dual luciferase reporter assay and electrophoretic mobility shift assay (EMSA). The dual luciferase reporter assay showed that the GA allele decreased the transcriptional efficiency by 10-fold (P < 0.001) compared with the G allele. Similarly, EMSA revealed that the GA allele had a weak transcription factor binding strength compared with the G allele. We then examined the frequency of this polymorphism in familial gastric cancer (FGC) patients by denaturing high-performance liquid chromatography. We found that the E-cadherin genotype (−347G/GA heterozygous or GA homozygous) was associated with FGC patients (P < 0.05) compared with the G homozygous genotype. Taken together, these results suggest that the GA allele may cause weak transcription factor binding affinity and low transcriptional activity in E-cadherin expression. |
| doi_str_mv | 10.1093/carcin/bgh073 |
| format | Article |
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Loss of E-cadherin expression in humans has been associated with cancer, and a number of cancer-related mutations have been identified. Here, we sought to investigate whether the −347G→GA single nucleotide polymorphism affects the transcriptional activity of the E-cadherin gene. First, we measured the promoter activity of the −347G→GA polymorphism using a dual luciferase reporter assay and electrophoretic mobility shift assay (EMSA). The dual luciferase reporter assay showed that the GA allele decreased the transcriptional efficiency by 10-fold (P < 0.001) compared with the G allele. Similarly, EMSA revealed that the GA allele had a weak transcription factor binding strength compared with the G allele. We then examined the frequency of this polymorphism in familial gastric cancer (FGC) patients by denaturing high-performance liquid chromatography. We found that the E-cadherin genotype (−347G/GA heterozygous or GA homozygous) was associated with FGC patients (P < 0.05) compared with the G homozygous genotype. Taken together, these results suggest that the GA allele may cause weak transcription factor binding affinity and low transcriptional activity in E-cadherin expression.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/bgh073</identifier><identifier>PMID: 14729585</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Alleles ; Biological and medical sciences ; Cadherins - genetics ; Carcinogenesis, carcinogens and anticarcinogens ; denaturing high-performance liquid chromatography ; DHPLC ; Electrophoretic Mobility Shift Assay ; EMSA ; familial gastric cancer ; FGC ; Gene Expression Regulation ; Gene Frequency ; Humans ; Medical sciences ; PCR–RFLP ; Polymerase Chain Reaction ; polymerase chain reaction–restriction fragment length polymorphism ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Promoter Regions, Genetic ; single nucleotide polymorphism ; SNP ; Transcription, Genetic ; Tumors</subject><ispartof>Carcinogenesis (New York), 2004-06, Vol.25 (6), p.895-899</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Jun 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-f7566a359df9ec38855b0a40735d4ff3eb8b515e214cd69ca55c928cdd9b2e8d3</citedby><cites>FETCH-LOGICAL-c423t-f7566a359df9ec38855b0a40735d4ff3eb8b515e214cd69ca55c928cdd9b2e8d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27915,27916</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15877965$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14729585$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shin, Yong</creatorcontrib><creatorcontrib>Kim, Il-Jin</creatorcontrib><creatorcontrib>Kang, Hio Chung</creatorcontrib><creatorcontrib>Park, Jae-Hyun</creatorcontrib><creatorcontrib>Park, Hye-Rin</creatorcontrib><creatorcontrib>Park, Hye-Won</creatorcontrib><creatorcontrib>Park, Mi Ae</creatorcontrib><creatorcontrib>Lee, Jong Soo</creatorcontrib><creatorcontrib>Yoon, Kyong-Ah</creatorcontrib><creatorcontrib>Ku, Ja-Lok</creatorcontrib><creatorcontrib>Park, Jae-Gahb</creatorcontrib><title>The E-cadherin −347G→GA promoter polymorphism and its effect on transcriptional regulation</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>E-cadherin plays a critical role in epithelial cell–cell adhesion and maintenance of tissue architecture. Loss of E-cadherin expression in humans has been associated with cancer, and a number of cancer-related mutations have been identified. Here, we sought to investigate whether the −347G→GA single nucleotide polymorphism affects the transcriptional activity of the E-cadherin gene. First, we measured the promoter activity of the −347G→GA polymorphism using a dual luciferase reporter assay and electrophoretic mobility shift assay (EMSA). The dual luciferase reporter assay showed that the GA allele decreased the transcriptional efficiency by 10-fold (P < 0.001) compared with the G allele. Similarly, EMSA revealed that the GA allele had a weak transcription factor binding strength compared with the G allele. We then examined the frequency of this polymorphism in familial gastric cancer (FGC) patients by denaturing high-performance liquid chromatography. We found that the E-cadherin genotype (−347G/GA heterozygous or GA homozygous) was associated with FGC patients (P < 0.05) compared with the G homozygous genotype. Taken together, these results suggest that the GA allele may cause weak transcription factor binding affinity and low transcriptional activity in E-cadherin expression.</description><subject>Alleles</subject><subject>Biological and medical sciences</subject><subject>Cadherins - genetics</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>denaturing high-performance liquid chromatography</subject><subject>DHPLC</subject><subject>Electrophoretic Mobility Shift Assay</subject><subject>EMSA</subject><subject>familial gastric cancer</subject><subject>FGC</subject><subject>Gene Expression Regulation</subject><subject>Gene Frequency</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>PCR–RFLP</subject><subject>Polymerase Chain Reaction</subject><subject>polymerase chain reaction–restriction fragment length polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Promoter Regions, Genetic</subject><subject>single nucleotide polymorphism</subject><subject>SNP</subject><subject>Transcription, Genetic</subject><subject>Tumors</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMtqGzEUhkVoiZ3LMtsiCl1OLY2kkbQMqS-BQC84JGQRodElVjq3SmNoXiBk7UfMk3SMTb06HM7HOf_5ALjA6CtGkkyMjiY0k_JphTg5AmNMC5TlWKAPYIwwJRkhhI7ASUrPCOGCMHkMRpjyXDLBxuBxuXJwmhltVy6GBr6_bQjl8_fXzfwSdrGt295F2LXVS93GbhVSDXVjYegTdN4708O2gX3UTTIxdH1oG13B6J7Wld42Z-Cj11Vy5_t6Cm5n0-XVIrv5Pr--urzJDM1Jn3nOikIP2ayXzhAhGCuRpsNHzFLviStFyTBzOabGFtJoxozMhbFWlrkTlpyCz7u9Q-Q_a5d69dyu45AlqRxLIigv8ABlO8jENqXovOpiqHV8URiprUy1k6l2Mgf-037puqydPdB7ewPwZQ_oZHTlBw0mpAPHBOeyYIfDIfXu7_-5jr9VwQlnanH_oJaLbz_vlrMf6hf5B6ZPkII</recordid><startdate>20040601</startdate><enddate>20040601</enddate><creator>Shin, Yong</creator><creator>Kim, Il-Jin</creator><creator>Kang, Hio Chung</creator><creator>Park, Jae-Hyun</creator><creator>Park, Hye-Rin</creator><creator>Park, Hye-Won</creator><creator>Park, Mi Ae</creator><creator>Lee, Jong Soo</creator><creator>Yoon, Kyong-Ah</creator><creator>Ku, Ja-Lok</creator><creator>Park, Jae-Gahb</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20040601</creationdate><title>The E-cadherin −347G→GA promoter polymorphism and its effect on transcriptional regulation</title><author>Shin, Yong ; Kim, Il-Jin ; Kang, Hio Chung ; Park, Jae-Hyun ; Park, Hye-Rin ; Park, Hye-Won ; Park, Mi Ae ; Lee, Jong Soo ; Yoon, Kyong-Ah ; Ku, Ja-Lok ; Park, Jae-Gahb</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-f7566a359df9ec38855b0a40735d4ff3eb8b515e214cd69ca55c928cdd9b2e8d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Alleles</topic><topic>Biological and medical sciences</topic><topic>Cadherins - genetics</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>denaturing high-performance liquid chromatography</topic><topic>DHPLC</topic><topic>Electrophoretic Mobility Shift Assay</topic><topic>EMSA</topic><topic>familial gastric cancer</topic><topic>FGC</topic><topic>Gene Expression Regulation</topic><topic>Gene Frequency</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>PCR–RFLP</topic><topic>Polymerase Chain Reaction</topic><topic>polymerase chain reaction–restriction fragment length polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Promoter Regions, Genetic</topic><topic>single nucleotide polymorphism</topic><topic>SNP</topic><topic>Transcription, Genetic</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shin, Yong</creatorcontrib><creatorcontrib>Kim, Il-Jin</creatorcontrib><creatorcontrib>Kang, Hio Chung</creatorcontrib><creatorcontrib>Park, Jae-Hyun</creatorcontrib><creatorcontrib>Park, Hye-Rin</creatorcontrib><creatorcontrib>Park, Hye-Won</creatorcontrib><creatorcontrib>Park, Mi Ae</creatorcontrib><creatorcontrib>Lee, Jong Soo</creatorcontrib><creatorcontrib>Yoon, Kyong-Ah</creatorcontrib><creatorcontrib>Ku, Ja-Lok</creatorcontrib><creatorcontrib>Park, Jae-Gahb</creatorcontrib><collection>Istex</collection><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>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shin, Yong</au><au>Kim, Il-Jin</au><au>Kang, Hio Chung</au><au>Park, Jae-Hyun</au><au>Park, Hye-Rin</au><au>Park, Hye-Won</au><au>Park, Mi Ae</au><au>Lee, Jong Soo</au><au>Yoon, Kyong-Ah</au><au>Ku, Ja-Lok</au><au>Park, Jae-Gahb</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The E-cadherin −347G→GA promoter polymorphism and its effect on transcriptional regulation</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2004-06-01</date><risdate>2004</risdate><volume>25</volume><issue>6</issue><spage>895</spage><epage>899</epage><pages>895-899</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>E-cadherin plays a critical role in epithelial cell–cell adhesion and maintenance of tissue architecture. Loss of E-cadherin expression in humans has been associated with cancer, and a number of cancer-related mutations have been identified. Here, we sought to investigate whether the −347G→GA single nucleotide polymorphism affects the transcriptional activity of the E-cadherin gene. First, we measured the promoter activity of the −347G→GA polymorphism using a dual luciferase reporter assay and electrophoretic mobility shift assay (EMSA). The dual luciferase reporter assay showed that the GA allele decreased the transcriptional efficiency by 10-fold (P < 0.001) compared with the G allele. Similarly, EMSA revealed that the GA allele had a weak transcription factor binding strength compared with the G allele. We then examined the frequency of this polymorphism in familial gastric cancer (FGC) patients by denaturing high-performance liquid chromatography. We found that the E-cadherin genotype (−347G/GA heterozygous or GA homozygous) was associated with FGC patients (P < 0.05) compared with the G homozygous genotype. Taken together, these results suggest that the GA allele may cause weak transcription factor binding affinity and low transcriptional activity in E-cadherin expression.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>14729585</pmid><doi>10.1093/carcin/bgh073</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Alleles Biological and medical sciences Cadherins - genetics Carcinogenesis, carcinogens and anticarcinogens denaturing high-performance liquid chromatography DHPLC Electrophoretic Mobility Shift Assay EMSA familial gastric cancer FGC Gene Expression Regulation Gene Frequency Humans Medical sciences PCR–RFLP Polymerase Chain Reaction polymerase chain reaction–restriction fragment length polymorphism Polymorphism, Genetic Polymorphism, Restriction Fragment Length Promoter Regions, Genetic single nucleotide polymorphism SNP Transcription, Genetic Tumors |
| title | The E-cadherin −347G→GA promoter polymorphism and its effect on transcriptional regulation |
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