Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9
A gene critical to esophageal cancer has been identified. Functional studies using microcell-mediated chromosome transfer of intact and truncated donor chromosomes 3 into an esophageal cancer cell line and nude mouse tumorigenicity assays were used to identify a 1.61 Mb tumor suppressive critical re...
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| Veröffentlicht in: | Oncogene 2007-01, Vol.26 (1), p.148-157 |
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| creator | Lo, P H Y Leung, A C C Kwok, C Y C Cheung, W S Y Ko, J M Y Yang, L C Law, S Wang, L D Li, J Stanbridge, E J Srivastava, G Tang, J C O Tsao, S W Lung, M L |
| description | A gene critical to esophageal cancer has been identified. Functional studies using microcell-mediated chromosome transfer of intact and truncated donor chromosomes 3 into an esophageal cancer cell line and nude mouse tumorigenicity assays were used to identify a 1.61 Mb tumor suppressive critical region (CR) mapping to chromosome 3p14.2. This CR is bounded by D3S1600 and D3S1285 microsatellite markers. One candidate tumor suppressor gene,
ADAMTS9,
maps to this CR. Further studies showed normal expression levels of this gene in tumor-suppressed microcell hybrids, levels that were much higher than observed in the recipient cells. Complete loss or downregulation of
ADAMTS9
gene expression was found in 15 out of 16 esophageal carcinoma cell lines. Promoter hypermethylation was detected in the cell lines that do not express this gene. Re-expression of
ADAMTS9
was observed after demethylation drug treatment, confirming that hypermethylation is involved in gene downregulation. Downregulation of
ADAMTS9
was also found in 43.5 and 47.6% of primary esophageal tumor tissues from Hong Kong and from the high-risk region of Henan, respectively. Thus, this study identifies and provides functional evidence for a CR associated with tumor suppression on 3p14.2 and provides the first evidence that
ADAMTS9
, mapping to this region, may contribute to esophageal cancer development. |
| doi_str_mv | 10.1038/sj.onc.1209767 |
| format | Article |
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ADAMTS9,
maps to this CR. Further studies showed normal expression levels of this gene in tumor-suppressed microcell hybrids, levels that were much higher than observed in the recipient cells. Complete loss or downregulation of
ADAMTS9
gene expression was found in 15 out of 16 esophageal carcinoma cell lines. Promoter hypermethylation was detected in the cell lines that do not express this gene. Re-expression of
ADAMTS9
was observed after demethylation drug treatment, confirming that hypermethylation is involved in gene downregulation. Downregulation of
ADAMTS9
was also found in 43.5 and 47.6% of primary esophageal tumor tissues from Hong Kong and from the high-risk region of Henan, respectively. Thus, this study identifies and provides functional evidence for a CR associated with tumor suppression on 3p14.2 and provides the first evidence that
ADAMTS9
, mapping to this region, may contribute to esophageal cancer development.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1209767</identifier><identifier>PMID: 16799631</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>ADAM Proteins - genetics ; ADAMTS9 Protein ; Apoptosis ; Base Sequence ; Biological and medical sciences ; Carcinoma, Squamous Cell - genetics ; Cell Biology ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Chromosome Mapping ; Chromosomes, Human, Pair 3 ; DNA ; DNA Methylation ; DNA sequencing ; Esophageal Neoplasms - genetics ; Esophagus ; Fundamental and applied biological sciences. Psychology ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes ; Genes, Tumor Suppressor ; Genetic aspects ; Head & neck cancer ; Health aspects ; Human Genetics ; Humans ; In Situ Hybridization, Fluorescence ; Internal Medicine ; Medical sciences ; Medicine ; Medicine & Public Health ; Molecular and cellular biology ; Molecular Sequence Data ; Nucleotide sequencing ; oncogenomics ; Oncology ; Squamous cell carcinoma ; Tumor suppressor genes ; Tumors</subject><ispartof>Oncogene, 2007-01, Vol.26 (1), p.148-157</ispartof><rights>Springer Nature Limited 2007</rights><rights>2007 INIST-CNRS</rights><rights>COPYRIGHT 2007 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 4, 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-57cf6c1f60808da8c90b6ade2278a7ae013828fe550543519a1cbe31e43316bc3</citedby><cites>FETCH-LOGICAL-c559t-57cf6c1f60808da8c90b6ade2278a7ae013828fe550543519a1cbe31e43316bc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.onc.1209767$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1209767$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18562507$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16799631$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lo, P H Y</creatorcontrib><creatorcontrib>Leung, A C C</creatorcontrib><creatorcontrib>Kwok, C Y C</creatorcontrib><creatorcontrib>Cheung, W S Y</creatorcontrib><creatorcontrib>Ko, J M Y</creatorcontrib><creatorcontrib>Yang, L C</creatorcontrib><creatorcontrib>Law, S</creatorcontrib><creatorcontrib>Wang, L D</creatorcontrib><creatorcontrib>Li, J</creatorcontrib><creatorcontrib>Stanbridge, E J</creatorcontrib><creatorcontrib>Srivastava, G</creatorcontrib><creatorcontrib>Tang, J C O</creatorcontrib><creatorcontrib>Tsao, S W</creatorcontrib><creatorcontrib>Lung, M L</creatorcontrib><title>Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>A gene critical to esophageal cancer has been identified. Functional studies using microcell-mediated chromosome transfer of intact and truncated donor chromosomes 3 into an esophageal cancer cell line and nude mouse tumorigenicity assays were used to identify a 1.61 Mb tumor suppressive critical region (CR) mapping to chromosome 3p14.2. This CR is bounded by D3S1600 and D3S1285 microsatellite markers. One candidate tumor suppressor gene,
ADAMTS9,
maps to this CR. Further studies showed normal expression levels of this gene in tumor-suppressed microcell hybrids, levels that were much higher than observed in the recipient cells. Complete loss or downregulation of
ADAMTS9
gene expression was found in 15 out of 16 esophageal carcinoma cell lines. Promoter hypermethylation was detected in the cell lines that do not express this gene. Re-expression of
ADAMTS9
was observed after demethylation drug treatment, confirming that hypermethylation is involved in gene downregulation. Downregulation of
ADAMTS9
was also found in 43.5 and 47.6% of primary esophageal tumor tissues from Hong Kong and from the high-risk region of Henan, respectively. Thus, this study identifies and provides functional evidence for a CR associated with tumor suppression on 3p14.2 and provides the first evidence that
ADAMTS9
, mapping to this region, may contribute to esophageal cancer development.</description><subject>ADAM Proteins - genetics</subject><subject>ADAMTS9 Protein</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Cell Biology</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Chromosome Mapping</subject><subject>Chromosomes, Human, Pair 3</subject><subject>DNA</subject><subject>DNA Methylation</subject><subject>DNA sequencing</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophagus</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genes, Tumor Suppressor</subject><subject>Genetic aspects</subject><subject>Head & neck cancer</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Internal Medicine</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular and cellular biology</subject><subject>Molecular Sequence Data</subject><subject>Nucleotide sequencing</subject><subject>oncogenomics</subject><subject>Oncology</subject><subject>Squamous cell carcinoma</subject><subject>Tumor suppressor genes</subject><subject>Tumors</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkl1rFDEUhgdR7Lp666UEi16523xMvi6X2mqh4oX1OmQzZ8YsO8k0mRH8Rf5NM-zCQqmUQBKS57znvPBW1VuC1wQzdZF36xjcmlCspZDPqgWppVhxruvn1QJrjleaMnpWvcp5hzGWGtOX1RkRUmvByKL6e9NAGH3rnR19DCi2yKJx6mNCeRqGBDn734Bc8mNB9ihBN2O9HQYfOjRGxAZSrynyAUGOwy_bQcHy_WT7OGXkYL9HzibnQ-wtsqFBeZwaD_nQypUX39gRHjQt1w4CfEKbz5tvdz_06-pFa_cZ3hzPZfXz-uru8uvq9vuXm8vN7coVz-OKS9cKR1qBFVaNVU7jrbANUCqVlRYwYYqqFjjHvGacaEvcFhiBmjEito4tq48H3SHF-wnyaHqfZxM2QPFjhKqxrJV-EqSEYUklfRIkutZMiVnx_QNwF6cUiltTxmdl3LIvq_MD1Nk9GB_aOCbrZkWzIUpjjimfpdaPUGU10HsXA7S-vD9W4FLMOUFrhuR7m_4Ygs0cNJN3pgTNHINWCt4dh522PTQn_JisAnw4AjaX4LTJBufziVNcUI5noYsDl8tX6CCdXP-n9T_T6OtN</recordid><startdate>20070104</startdate><enddate>20070104</enddate><creator>Lo, P H Y</creator><creator>Leung, A C C</creator><creator>Kwok, C Y C</creator><creator>Cheung, W S Y</creator><creator>Ko, J M Y</creator><creator>Yang, L C</creator><creator>Law, S</creator><creator>Wang, L D</creator><creator>Li, J</creator><creator>Stanbridge, E J</creator><creator>Srivastava, G</creator><creator>Tang, J C O</creator><creator>Tsao, S W</creator><creator>Lung, M L</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</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>FR3</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>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20070104</creationdate><title>Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9</title><author>Lo, P H Y ; Leung, A C C ; Kwok, C Y C ; Cheung, W S Y ; Ko, J M Y ; Yang, L C ; Law, S ; Wang, L D ; Li, J ; Stanbridge, E J ; Srivastava, G ; Tang, J C O ; Tsao, S W ; Lung, M L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559t-57cf6c1f60808da8c90b6ade2278a7ae013828fe550543519a1cbe31e43316bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>ADAM Proteins - genetics</topic><topic>ADAMTS9 Protein</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Cell Biology</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Chromosome Mapping</topic><topic>Chromosomes, Human, Pair 3</topic><topic>DNA</topic><topic>DNA Methylation</topic><topic>DNA sequencing</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophagus</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Genes, Tumor Suppressor</topic><topic>Genetic aspects</topic><topic>Head & neck cancer</topic><topic>Health aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Internal Medicine</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular and cellular biology</topic><topic>Molecular Sequence Data</topic><topic>Nucleotide sequencing</topic><topic>oncogenomics</topic><topic>Oncology</topic><topic>Squamous cell carcinoma</topic><topic>Tumor suppressor genes</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lo, P H Y</creatorcontrib><creatorcontrib>Leung, A C C</creatorcontrib><creatorcontrib>Kwok, C Y C</creatorcontrib><creatorcontrib>Cheung, W S Y</creatorcontrib><creatorcontrib>Ko, J M Y</creatorcontrib><creatorcontrib>Yang, L C</creatorcontrib><creatorcontrib>Law, S</creatorcontrib><creatorcontrib>Wang, L D</creatorcontrib><creatorcontrib>Li, J</creatorcontrib><creatorcontrib>Stanbridge, E J</creatorcontrib><creatorcontrib>Srivastava, G</creatorcontrib><creatorcontrib>Tang, J C O</creatorcontrib><creatorcontrib>Tsao, S W</creatorcontrib><creatorcontrib>Lung, M L</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lo, P H Y</au><au>Leung, A C C</au><au>Kwok, C Y C</au><au>Cheung, W S Y</au><au>Ko, J M Y</au><au>Yang, L C</au><au>Law, S</au><au>Wang, L D</au><au>Li, J</au><au>Stanbridge, E J</au><au>Srivastava, G</au><au>Tang, J C O</au><au>Tsao, S W</au><au>Lung, M L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2007-01-04</date><risdate>2007</risdate><volume>26</volume><issue>1</issue><spage>148</spage><epage>157</epage><pages>148-157</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>A gene critical to esophageal cancer has been identified. Functional studies using microcell-mediated chromosome transfer of intact and truncated donor chromosomes 3 into an esophageal cancer cell line and nude mouse tumorigenicity assays were used to identify a 1.61 Mb tumor suppressive critical region (CR) mapping to chromosome 3p14.2. This CR is bounded by D3S1600 and D3S1285 microsatellite markers. One candidate tumor suppressor gene,
ADAMTS9,
maps to this CR. Further studies showed normal expression levels of this gene in tumor-suppressed microcell hybrids, levels that were much higher than observed in the recipient cells. Complete loss or downregulation of
ADAMTS9
gene expression was found in 15 out of 16 esophageal carcinoma cell lines. Promoter hypermethylation was detected in the cell lines that do not express this gene. Re-expression of
ADAMTS9
was observed after demethylation drug treatment, confirming that hypermethylation is involved in gene downregulation. Downregulation of
ADAMTS9
was also found in 43.5 and 47.6% of primary esophageal tumor tissues from Hong Kong and from the high-risk region of Henan, respectively. Thus, this study identifies and provides functional evidence for a CR associated with tumor suppression on 3p14.2 and provides the first evidence that
ADAMTS9
, mapping to this region, may contribute to esophageal cancer development.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>16799631</pmid><doi>10.1038/sj.onc.1209767</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncogene, 2007-01, Vol.26 (1), p.148-157 |
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| source | MEDLINE; Nature; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SpringerLink Journals - AutoHoldings |
| subjects | ADAM Proteins - genetics ADAMTS9 Protein Apoptosis Base Sequence Biological and medical sciences Carcinoma, Squamous Cell - genetics Cell Biology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chromosome Mapping Chromosomes, Human, Pair 3 DNA DNA Methylation DNA sequencing Esophageal Neoplasms - genetics Esophagus Fundamental and applied biological sciences. Psychology Gastroenterology. Liver. Pancreas. Abdomen Gene expression Gene Expression Regulation, Neoplastic Genes Genes, Tumor Suppressor Genetic aspects Head & neck cancer Health aspects Human Genetics Humans In Situ Hybridization, Fluorescence Internal Medicine Medical sciences Medicine Medicine & Public Health Molecular and cellular biology Molecular Sequence Data Nucleotide sequencing oncogenomics Oncology Squamous cell carcinoma Tumor suppressor genes Tumors |
| title | Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9 |
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