Dickkopf-3/REIC functions as a suppressor gene of tumor growth
To identify putative tumor suppressor genes in hepatocarcinogenesis, we combined the representational difference analysis and reverse northern blot identifying downregulated genes in human hepatoma tissues. One of them was Dkk-3/REIC . Dkk-3/REIC was downregulated in 11 out of the 20 human hepatoma...
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| Veröffentlicht in: | Oncogene 2004-12, Vol.23 (57), p.9183-9189 |
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| creator | Hsieh, Sen-Yung Hsieh, Pei-Shan Chiu, Cheng-Tang Chen, Wai-Ying |
| description | To identify putative tumor suppressor genes in hepatocarcinogenesis, we combined the representational difference analysis and reverse northern blot identifying downregulated genes in human hepatoma tissues. One of them was
Dkk-3/REIC
.
Dkk-3/REIC
was downregulated in 11 out of the 20 human hepatoma tissues as compared to their counterparts of noncancerous liver tissues by northern blot analysis. It was also downregulated in 29 out of 48 human cancer samples including the kidney, urinary bladder, prostate, pancreas and lung cancers. Its gene product, Dkk-3/REIC, was found to be N-glycosylated and have two isoforms, the 55 kDa in the cytosol and 50 kDa secreted in the medium. Ectopic expression of
Dkk-3/REIC
in HeLa, Hep3B and Huh 7 cells led to suppression of cell growth, which was primarily attributable to induction of cell apoptosis. The suppression phenomenon was found to be cell-type related (most prominent in HeLa and least in Hep3B cells) and cell-density dependent (attenuated as the cell density increased). Transduction of
Dkk-3/REIC
into HeLa and Hep3B cells caused suppression on colony formation
in vitro
and reduced tumor growth rate in inoculated athymic nude mice. In conclusion, these data indicate that Dkk-3/REIC functions as a suppressor for human tumor growth. |
| doi_str_mv | 10.1038/sj.onc.1208138 |
| format | Article |
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Dkk-3/REIC
.
Dkk-3/REIC
was downregulated in 11 out of the 20 human hepatoma tissues as compared to their counterparts of noncancerous liver tissues by northern blot analysis. It was also downregulated in 29 out of 48 human cancer samples including the kidney, urinary bladder, prostate, pancreas and lung cancers. Its gene product, Dkk-3/REIC, was found to be N-glycosylated and have two isoforms, the 55 kDa in the cytosol and 50 kDa secreted in the medium. Ectopic expression of
Dkk-3/REIC
in HeLa, Hep3B and Huh 7 cells led to suppression of cell growth, which was primarily attributable to induction of cell apoptosis. The suppression phenomenon was found to be cell-type related (most prominent in HeLa and least in Hep3B cells) and cell-density dependent (attenuated as the cell density increased). Transduction of
Dkk-3/REIC
into HeLa and Hep3B cells caused suppression on colony formation
in vitro
and reduced tumor growth rate in inoculated athymic nude mice. In conclusion, these data indicate that Dkk-3/REIC functions as a suppressor for human tumor growth.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1208138</identifier><identifier>PMID: 15516983</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Amino Acid Sequence ; Apoptosis ; Base Sequence ; Biological and medical sciences ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - pathology ; Cell Biology ; Cell density ; Cell Division - genetics ; Cell growth ; Cell Line, Tumor ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cytosol ; DNA Primers ; Ectopic expression ; Fundamental and applied biological sciences. Psychology ; Gastroenterology. Liver. Pancreas. Abdomen ; Genes ; Genes, Tumor Suppressor ; Glycosylation ; Growth rate ; Hepatoma ; Human Genetics ; Humans ; Intercellular Signaling Peptides and Proteins ; Internal Medicine ; Isoforms ; Kidneys ; Kinases ; Liver cancer ; Liver Neoplasms - genetics ; Liver Neoplasms - pathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Loss of Heterozygosity ; Medical sciences ; Medicine ; Medicine & Public Health ; Molecular and cellular biology ; Molecular Sequence Data ; Oncology ; original-paper ; Prostate ; Proteins - genetics ; Proteins - physiology ; Tumor suppressor genes ; Tumors ; Urinary bladder</subject><ispartof>Oncogene, 2004-12, Vol.23 (57), p.9183-9189</ispartof><rights>Springer Nature Limited 2004</rights><rights>2005 INIST-CNRS</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 9, 2004</rights><rights>Nature Publishing Group 2004.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c622t-4fd193f015dbeb4376b888327e0701d04069799e2a962d45b0b5266e6991b4913</citedby><cites>FETCH-LOGICAL-c622t-4fd193f015dbeb4376b888327e0701d04069799e2a962d45b0b5266e6991b4913</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.1208138$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1208138$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16338808$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15516983$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hsieh, Sen-Yung</creatorcontrib><creatorcontrib>Hsieh, Pei-Shan</creatorcontrib><creatorcontrib>Chiu, Cheng-Tang</creatorcontrib><creatorcontrib>Chen, Wai-Ying</creatorcontrib><title>Dickkopf-3/REIC functions as a suppressor gene of tumor growth</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>To identify putative tumor suppressor genes in hepatocarcinogenesis, we combined the representational difference analysis and reverse northern blot identifying downregulated genes in human hepatoma tissues. One of them was
Dkk-3/REIC
.
Dkk-3/REIC
was downregulated in 11 out of the 20 human hepatoma tissues as compared to their counterparts of noncancerous liver tissues by northern blot analysis. It was also downregulated in 29 out of 48 human cancer samples including the kidney, urinary bladder, prostate, pancreas and lung cancers. Its gene product, Dkk-3/REIC, was found to be N-glycosylated and have two isoforms, the 55 kDa in the cytosol and 50 kDa secreted in the medium. Ectopic expression of
Dkk-3/REIC
in HeLa, Hep3B and Huh 7 cells led to suppression of cell growth, which was primarily attributable to induction of cell apoptosis. The suppression phenomenon was found to be cell-type related (most prominent in HeLa and least in Hep3B cells) and cell-density dependent (attenuated as the cell density increased). Transduction of
Dkk-3/REIC
into HeLa and Hep3B cells caused suppression on colony formation
in vitro
and reduced tumor growth rate in inoculated athymic nude mice. In conclusion, these data indicate that Dkk-3/REIC functions as a suppressor for human tumor growth.</description><subject>Amino Acid Sequence</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell Biology</subject><subject>Cell density</subject><subject>Cell Division - genetics</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cytosol</subject><subject>DNA Primers</subject><subject>Ectopic expression</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genes</subject><subject>Genes, Tumor Suppressor</subject><subject>Glycosylation</subject><subject>Growth rate</subject><subject>Hepatoma</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins</subject><subject>Internal Medicine</subject><subject>Isoforms</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - pathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Loss of Heterozygosity</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>Oncology</subject><subject>original-paper</subject><subject>Prostate</subject><subject>Proteins - genetics</subject><subject>Proteins - physiology</subject><subject>Tumor suppressor genes</subject><subject>Tumors</subject><subject>Urinary bladder</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</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>eNqFkd2L1DAUxYMo7jj66qMURd86k--Pl4VlXHVhQRB9DmmajJ1tk5q0iP-9KVsYkF0kgZDkd8-9hwPAawR3CBK5z6ddDHaHMJSIyCdgg6jgNWOKPgUbqBisFSb4ArzI-QQhFAri5-ACMYa4kmQDLj929u4ujr4m-2_XN4fKz8FOXQy5MmVXeR7H5HKOqTq64Kroq2kelluKv6efL8Ezb_rsXq3nFvz4dP398KW-_fr55nB1W1uO8VRT3yJFPESsbVxDieCNlJJg4aCAqIUUciWUctgojlvKGtgwzLnjSqGGKkS24MO97pjir9nlSQ9dtq7vTXBxzpoLpCCi7L8gEoJiJhbFd_-ApzinUExozCkiRNAy8ha8fZTCghBJKTxLHU3vdBd8nJKxS199haSCQnCOC7V7gCqrdUNnY3C-K-8PFdgUc07O6zF1g0l_NIJ6CV_nky7h6zX8UvBmHXZuBtee8TXtArxfAZOt6X0ywXb5zPFiSMJFaH_P5fIVji6dXT_S-i_x4cHE</recordid><startdate>20041209</startdate><enddate>20041209</enddate><creator>Hsieh, Sen-Yung</creator><creator>Hsieh, Pei-Shan</creator><creator>Chiu, Cheng-Tang</creator><creator>Chen, Wai-Ying</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>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20041209</creationdate><title>Dickkopf-3/REIC functions as a suppressor gene of tumor growth</title><author>Hsieh, Sen-Yung ; Hsieh, Pei-Shan ; Chiu, Cheng-Tang ; Chen, Wai-Ying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c622t-4fd193f015dbeb4376b888327e0701d04069799e2a962d45b0b5266e6991b4913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Amino Acid Sequence</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell Biology</topic><topic>Cell density</topic><topic>Cell Division - genetics</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cytosol</topic><topic>DNA Primers</topic><topic>Ectopic expression</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genes</topic><topic>Genes, Tumor Suppressor</topic><topic>Glycosylation</topic><topic>Growth rate</topic><topic>Hepatoma</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins</topic><topic>Internal Medicine</topic><topic>Isoforms</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - pathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Loss of Heterozygosity</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>Oncology</topic><topic>original-paper</topic><topic>Prostate</topic><topic>Proteins - genetics</topic><topic>Proteins - physiology</topic><topic>Tumor suppressor genes</topic><topic>Tumors</topic><topic>Urinary bladder</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hsieh, Sen-Yung</creatorcontrib><creatorcontrib>Hsieh, Pei-Shan</creatorcontrib><creatorcontrib>Chiu, Cheng-Tang</creatorcontrib><creatorcontrib>Chen, Wai-Ying</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 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>Hsieh, Sen-Yung</au><au>Hsieh, Pei-Shan</au><au>Chiu, Cheng-Tang</au><au>Chen, Wai-Ying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dickkopf-3/REIC functions as a suppressor gene of tumor growth</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2004-12-09</date><risdate>2004</risdate><volume>23</volume><issue>57</issue><spage>9183</spage><epage>9189</epage><pages>9183-9189</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>To identify putative tumor suppressor genes in hepatocarcinogenesis, we combined the representational difference analysis and reverse northern blot identifying downregulated genes in human hepatoma tissues. One of them was
Dkk-3/REIC
.
Dkk-3/REIC
was downregulated in 11 out of the 20 human hepatoma tissues as compared to their counterparts of noncancerous liver tissues by northern blot analysis. It was also downregulated in 29 out of 48 human cancer samples including the kidney, urinary bladder, prostate, pancreas and lung cancers. Its gene product, Dkk-3/REIC, was found to be N-glycosylated and have two isoforms, the 55 kDa in the cytosol and 50 kDa secreted in the medium. Ectopic expression of
Dkk-3/REIC
in HeLa, Hep3B and Huh 7 cells led to suppression of cell growth, which was primarily attributable to induction of cell apoptosis. The suppression phenomenon was found to be cell-type related (most prominent in HeLa and least in Hep3B cells) and cell-density dependent (attenuated as the cell density increased). Transduction of
Dkk-3/REIC
into HeLa and Hep3B cells caused suppression on colony formation
in vitro
and reduced tumor growth rate in inoculated athymic nude mice. In conclusion, these data indicate that Dkk-3/REIC functions as a suppressor for human tumor growth.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15516983</pmid><doi>10.1038/sj.onc.1208138</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; Nature Journals Online; EZB-FREE-00999 freely available EZB journals; SpringerLink Journals - AutoHoldings |
| subjects | Amino Acid Sequence Apoptosis Base Sequence Biological and medical sciences Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - pathology Cell Biology Cell density Cell Division - genetics Cell growth Cell Line, Tumor Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cytosol DNA Primers Ectopic expression Fundamental and applied biological sciences. Psychology Gastroenterology. Liver. Pancreas. Abdomen Genes Genes, Tumor Suppressor Glycosylation Growth rate Hepatoma Human Genetics Humans Intercellular Signaling Peptides and Proteins Internal Medicine Isoforms Kidneys Kinases Liver cancer Liver Neoplasms - genetics Liver Neoplasms - pathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Loss of Heterozygosity Medical sciences Medicine Medicine & Public Health Molecular and cellular biology Molecular Sequence Data Oncology original-paper Prostate Proteins - genetics Proteins - physiology Tumor suppressor genes Tumors Urinary bladder |
| title | Dickkopf-3/REIC functions as a suppressor gene of tumor growth |
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