Truncation of the TGF-β type II receptor gene results in insensitivity to TGF-β in human gastric cancer cells
The transforming growth factor-beta (TGF-beta receptor system has been implicated in the development of resistance to the growth-inhibitory effects of TGF-beta. It has been reported that resistance to TGF-beta correlates with inactivation of the TGF-beta type II receptor (RII). In the present report...
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| Veröffentlicht in: | Oncogene 1999-04, Vol.18 (13), p.2213-2219 |
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| creator | YANG, H.-K SHIN HYEOK KANG KIM, Y.-S KYUNGSHICK WON BANG, Y.-J KIM, S.-J |
| description | The transforming growth factor-beta (TGF-beta receptor system has been implicated in the development of resistance to the growth-inhibitory effects of TGF-beta. It has been reported that resistance to TGF-beta correlates with inactivation of the TGF-beta type II receptor (RII). In the present report, we examine the genetic changes in the TGF-beta RII gene of human gastric cancer cell lines, SNU-5 and SNU-668, which we had previously reported to express truncated TGF-beta RII transcripts. By independent PCR and Southern hybridization analysis of genomic DNA, we found that the genomic sequence of TGF-beta RII is truncated after exon 2 in SNU-5 and after exon 3 in SNU-668. This was confirmed by sequencing the TGF-beta RII cDNA cloned from a SNU-5 cDNA library. Predicted TGF-beta RII protein of SNU-5 cells based on sequencing data contains only a part of extracellular domain of TGF-beta RII. We demonstrate that cotransfection of 3TP-Lux and wild type TGF-beta RII restores the TGF-beta responsiveness in SNU-5 cells, suggesting that genetic changes in the TGF-beta RII gene of SNU-5 cells are responsible for the loss of sensitivity to TGF-beta. This is the first report demonstrating that truncation of the TGF-beta RII gene is an alternative mechanism to inactivate the TGF-beta signal transduction pathways. |
| doi_str_mv | 10.1038/sj.onc.1202535 |
| format | Article |
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It has been reported that resistance to TGF-beta correlates with inactivation of the TGF-beta type II receptor (RII). In the present report, we examine the genetic changes in the TGF-beta RII gene of human gastric cancer cell lines, SNU-5 and SNU-668, which we had previously reported to express truncated TGF-beta RII transcripts. By independent PCR and Southern hybridization analysis of genomic DNA, we found that the genomic sequence of TGF-beta RII is truncated after exon 2 in SNU-5 and after exon 3 in SNU-668. This was confirmed by sequencing the TGF-beta RII cDNA cloned from a SNU-5 cDNA library. Predicted TGF-beta RII protein of SNU-5 cells based on sequencing data contains only a part of extracellular domain of TGF-beta RII. We demonstrate that cotransfection of 3TP-Lux and wild type TGF-beta RII restores the TGF-beta responsiveness in SNU-5 cells, suggesting that genetic changes in the TGF-beta RII gene of SNU-5 cells are responsible for the loss of sensitivity to TGF-beta. This is the first report demonstrating that truncation of the TGF-beta RII gene is an alternative mechanism to inactivate the TGF-beta signal transduction pathways.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1202535</identifier><identifier>PMID: 10327067</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Amino Acid Sequence ; Base Sequence ; Biological and medical sciences ; Blotting, Southern ; Carcinoma - genetics ; Carcinoma - metabolism ; Carcinoma - pathology ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; DNA, Neoplasm - genetics ; Fundamental and applied biological sciences. Psychology ; Gastric cancer ; Genomic analysis ; Humans ; Hybridization analysis ; Molecular and cellular biology ; Molecular Sequence Data ; Neoplasm Proteins - genetics ; Neoplasm Proteins - physiology ; Nucleotide sequence ; Physical growth ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases ; Receptors, Transforming Growth Factor beta - genetics ; Receptors, Transforming Growth Factor beta - physiology ; RNA, Messenger - genetics ; RNA, Neoplasm - genetics ; Sequence Deletion ; Signal transduction ; Signal Transduction - genetics ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology ; Transforming Growth Factor beta - pharmacology ; Transforming growth factor-b ; Tumor cell lines ; Tumor Cells, Cultured</subject><ispartof>Oncogene, 1999-04, Vol.18 (13), p.2213-2219</ispartof><rights>1999 INIST-CNRS</rights><rights>Macmillan Publishers Limited 1999.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c379t-f8243f000a2eae00fc5ae11bb458bd7159784c2c135fb364eee496a4b1c6d7513</citedby><cites>FETCH-LOGICAL-c379t-f8243f000a2eae00fc5ae11bb458bd7159784c2c135fb364eee496a4b1c6d7513</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1770053$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10327067$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YANG, H.-K</creatorcontrib><creatorcontrib>SHIN HYEOK KANG</creatorcontrib><creatorcontrib>KIM, Y.-S</creatorcontrib><creatorcontrib>KYUNGSHICK WON</creatorcontrib><creatorcontrib>BANG, Y.-J</creatorcontrib><creatorcontrib>KIM, S.-J</creatorcontrib><title>Truncation of the TGF-β type II receptor gene results in insensitivity to TGF-β in human gastric cancer cells</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>The transforming growth factor-beta (TGF-beta receptor system has been implicated in the development of resistance to the growth-inhibitory effects of TGF-beta. 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This is the first report demonstrating that truncation of the TGF-beta RII gene is an alternative mechanism to inactivate the TGF-beta signal transduction pathways.</description><subject>Amino Acid Sequence</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Blotting, Southern</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - metabolism</subject><subject>Carcinoma - pathology</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>DNA, Neoplasm - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastric cancer</subject><subject>Genomic analysis</subject><subject>Humans</subject><subject>Hybridization analysis</subject><subject>Molecular and cellular biology</subject><subject>Molecular Sequence Data</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - physiology</subject><subject>Nucleotide sequence</subject><subject>Physical growth</subject><subject>Polymerase Chain Reaction</subject><subject>Protein-Serine-Threonine Kinases</subject><subject>Receptors, Transforming Growth Factor beta - genetics</subject><subject>Receptors, Transforming Growth Factor beta - physiology</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Neoplasm - genetics</subject><subject>Sequence Deletion</subject><subject>Signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>Transforming growth factor-b</subject><subject>Tumor cell lines</subject><subject>Tumor Cells, Cultured</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc9qGzEQxkVpaNy01x6LoKW3dfV3tXssoUkNgVycs9DKs4nMWnI12oJfKw_SZ4qMXVoKA8Mwv2_4mI-QD5wtOZPdV9wuU_RLLpjQUr8iC65M22jdq9dkwXrNml5IcUneIm4ZY6Zn4g25rFJhWGsWJK3zHL0rIUWaRlqegK5vb5rfz7Qc9kBXK5rBw76kTB8hQp1wngrSEGshRAwl_ArlQEv6I6yrp3nnIn10WHLw1LvoIVMP04TvyMXoJoT3535FHm6-r69_NHf3t6vrb3eNl6YvzdgJJcdq2AlwwNjotQPOh0HpbtgYrnvTKS88l3ocZKsAQPWtUwP37cZoLq_Il9PdfU4_Z8BidwGPDlyENKPlRkjWma6Cn_4Dt2nOsXqzolVc9EyJI7U8UT4nxAyj3eewc_lgObPHICxubQ3CnoOogo_ns_Owg80_-OnzFfh8Bhx6N425PingX84YxrSUL4_LkiI</recordid><startdate>19990401</startdate><enddate>19990401</enddate><creator>YANG, H.-K</creator><creator>SHIN HYEOK KANG</creator><creator>KIM, Y.-S</creator><creator>KYUNGSHICK WON</creator><creator>BANG, Y.-J</creator><creator>KIM, S.-J</creator><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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>19990401</creationdate><title>Truncation of the TGF-β type II receptor gene results in insensitivity to TGF-β in human gastric cancer cells</title><author>YANG, H.-K ; SHIN HYEOK KANG ; KIM, Y.-S ; KYUNGSHICK WON ; BANG, Y.-J ; KIM, S.-J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c379t-f8243f000a2eae00fc5ae11bb458bd7159784c2c135fb364eee496a4b1c6d7513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Amino Acid Sequence</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Blotting, Southern</topic><topic>Carcinoma - genetics</topic><topic>Carcinoma - metabolism</topic><topic>Carcinoma - pathology</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>DNA, Neoplasm - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gastric cancer</topic><topic>Genomic analysis</topic><topic>Humans</topic><topic>Hybridization analysis</topic><topic>Molecular and cellular biology</topic><topic>Molecular Sequence Data</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - physiology</topic><topic>Nucleotide sequence</topic><topic>Physical growth</topic><topic>Polymerase Chain Reaction</topic><topic>Protein-Serine-Threonine Kinases</topic><topic>Receptors, Transforming Growth Factor beta - genetics</topic><topic>Receptors, Transforming Growth Factor beta - physiology</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Neoplasm - genetics</topic><topic>Sequence Deletion</topic><topic>Signal transduction</topic><topic>Signal Transduction - genetics</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><topic>Transforming Growth Factor beta - pharmacology</topic><topic>Transforming growth factor-b</topic><topic>Tumor cell lines</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YANG, H.-K</creatorcontrib><creatorcontrib>SHIN HYEOK KANG</creatorcontrib><creatorcontrib>KIM, Y.-S</creatorcontrib><creatorcontrib>KYUNGSHICK WON</creatorcontrib><creatorcontrib>BANG, Y.-J</creatorcontrib><creatorcontrib>KIM, S.-J</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</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>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YANG, H.-K</au><au>SHIN HYEOK KANG</au><au>KIM, Y.-S</au><au>KYUNGSHICK WON</au><au>BANG, Y.-J</au><au>KIM, S.-J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Truncation of the TGF-β type II receptor gene results in insensitivity to TGF-β in human gastric cancer cells</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>1999-04-01</date><risdate>1999</risdate><volume>18</volume><issue>13</issue><spage>2213</spage><epage>2219</epage><pages>2213-2219</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>The transforming growth factor-beta (TGF-beta receptor system has been implicated in the development of resistance to the growth-inhibitory effects of TGF-beta. It has been reported that resistance to TGF-beta correlates with inactivation of the TGF-beta type II receptor (RII). In the present report, we examine the genetic changes in the TGF-beta RII gene of human gastric cancer cell lines, SNU-5 and SNU-668, which we had previously reported to express truncated TGF-beta RII transcripts. By independent PCR and Southern hybridization analysis of genomic DNA, we found that the genomic sequence of TGF-beta RII is truncated after exon 2 in SNU-5 and after exon 3 in SNU-668. This was confirmed by sequencing the TGF-beta RII cDNA cloned from a SNU-5 cDNA library. Predicted TGF-beta RII protein of SNU-5 cells based on sequencing data contains only a part of extracellular domain of TGF-beta RII. We demonstrate that cotransfection of 3TP-Lux and wild type TGF-beta RII restores the TGF-beta responsiveness in SNU-5 cells, suggesting that genetic changes in the TGF-beta RII gene of SNU-5 cells are responsible for the loss of sensitivity to TGF-beta. This is the first report demonstrating that truncation of the TGF-beta RII gene is an alternative mechanism to inactivate the TGF-beta signal transduction pathways.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>10327067</pmid><doi>10.1038/sj.onc.1202535</doi><tpages>7</tpages></addata></record> |
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| ispartof | Oncogene, 1999-04, Vol.18 (13), p.2213-2219 |
| issn | 0950-9232 1476-5594 |
| 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 Base Sequence Biological and medical sciences Blotting, Southern Carcinoma - genetics Carcinoma - metabolism Carcinoma - pathology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes DNA, Neoplasm - genetics Fundamental and applied biological sciences. Psychology Gastric cancer Genomic analysis Humans Hybridization analysis Molecular and cellular biology Molecular Sequence Data Neoplasm Proteins - genetics Neoplasm Proteins - physiology Nucleotide sequence Physical growth Polymerase Chain Reaction Protein-Serine-Threonine Kinases Receptors, Transforming Growth Factor beta - genetics Receptors, Transforming Growth Factor beta - physiology RNA, Messenger - genetics RNA, Neoplasm - genetics Sequence Deletion Signal transduction Signal Transduction - genetics Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Transforming Growth Factor beta - pharmacology Transforming growth factor-b Tumor cell lines Tumor Cells, Cultured |
| title | Truncation of the TGF-β type II receptor gene results in insensitivity to TGF-β in human gastric cancer cells |
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