The topoisomerase I- and p53-binding protein topors is differentially expressed in normal and malignant human tissues and may function as a tumor suppressor
Topors was identified recently as a human protein that binds to topoisomerase I and p53. Topors contains a highly conserved RING domain and localizes in promyelocytic leukemia nuclear bodies. Relatively little is known regarding topors expression patterns or function. We now demonstrate that topors...
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| Veröffentlicht in: | Oncogene 2004-07, Vol.23 (31), p.5293-5300 |
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| creator | Saleem, Ahamed Dutta, Jayeeta Malegaonkar, Diptee Rasheed, Farheena Rasheed, Zeshaan Rajendra, Rajeev Marshall, Henderson Luo, Minje Li, Honghua Rubin, Eric H |
| description | Topors was identified recently as a human protein that binds to topoisomerase I and p53. Topors contains a highly conserved RING domain and localizes in promyelocytic leukemia nuclear bodies. Relatively little is known regarding topors expression patterns or function. We now demonstrate that topors mRNA and protein are widely expressed in normal human tissues. By contrast, topors mRNA and protein levels are decreased or undetectable in colon adenocarcinomas relative to normal colon tissue, and expression of the topors protein is not detectable in several colon cancer cell lines. The human
TOPORS
gene is located on chromosome 9p21, with loss of heterozygosity in this region frequently observed in several different malignancies. While we were unable to detect loss of heterozygosity of the
TOPORS
gene in 16 sporadic colon cancer cases, increased methylation of a CpG island in the
TOPORS
promoter was evident in colon adenocarcinoma specimens relative to matched normal tissues. Additional studies indicate that forced expression of topors inhibits cellular proliferation and is associated with an accumulation of cells in the G
0
/G
1
phase of the cell cycle. This effect is independent of the topors RING domain and maps to a C-terminal region of the protein. These results suggest that topors functions as a negative regulator of cell growth, and possibly as a tumor suppressor. |
| doi_str_mv | 10.1038/sj.onc.1207700 |
| format | Article |
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TOPORS
gene is located on chromosome 9p21, with loss of heterozygosity in this region frequently observed in several different malignancies. While we were unable to detect loss of heterozygosity of the
TOPORS
gene in 16 sporadic colon cancer cases, increased methylation of a CpG island in the
TOPORS
promoter was evident in colon adenocarcinoma specimens relative to matched normal tissues. Additional studies indicate that forced expression of topors inhibits cellular proliferation and is associated with an accumulation of cells in the G
0
/G
1
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TOPORS
gene is located on chromosome 9p21, with loss of heterozygosity in this region frequently observed in several different malignancies. While we were unable to detect loss of heterozygosity of the
TOPORS
gene in 16 sporadic colon cancer cases, increased methylation of a CpG island in the
TOPORS
promoter was evident in colon adenocarcinoma specimens relative to matched normal tissues. Additional studies indicate that forced expression of topors inhibits cellular proliferation and is associated with an accumulation of cells in the G
0
/G
1
phase of the cell cycle. This effect is independent of the topors RING domain and maps to a C-terminal region of the protein. These results suggest that topors functions as a negative regulator of cell growth, and possibly as a tumor suppressor.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - metabolism</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Carrier Proteins - biosynthesis</subject><subject>Cell Biology</subject><subject>Cell Cycle</subject><subject>Cell Division</subject><subject>Cell physiology</subject><subject>Cell proliferation</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Chromosome 9</subject><subject>Colon - metabolism</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colorectal cancer</subject><subject>CpG Islands</subject><subject>Dentistry</subject><subject>DNA Methylation</subject><subject>DNA topoisomerase</subject><subject>DNA-Binding Proteins - biosynthesis</subject><subject>Flow Cytometry</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>G1 Phase</subject><subject>Gene mapping</subject><subject>Genes, Tumor Suppressor</subject><subject>Green Fluorescent Proteins</subject><subject>HeLa Cells</subject><subject>Heterozygosity</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Leukemia</subject><subject>Loss of Heterozygosity</subject><subject>Luminescent Proteins - metabolism</subject><subject>Medical schools</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular and cellular biology</subject><subject>mRNA</subject><subject>Neoplasm Proteins</subject><subject>Nuclear Proteins - biosynthesis</subject><subject>Oncology</subject><subject>original-paper</subject><subject>p53 Protein</subject><subject>Promyeloid leukemia</subject><subject>Protein Structure, Tertiary</subject><subject>Proteins</subject><subject>Resting Phase, Cell Cycle</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Thymidine - metabolism</subject><subject>Time Factors</subject><subject>Tissue Distribution</subject><subject>Transcription Factors - biosynthesis</subject><subject>Tumor cell lines</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><subject>U937 Cells</subject><subject>Ubiquitin-Protein Ligases - metabolism</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>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkk9r3DAQxU1pabbbXnssoqW9eaO_1uoYQtIGAr2kZyHLo40WW3IlG7rfpR-2ysawpSQUHQY0v3kzD15VvSd4QzDbnuf9Jga7IRRLifGLakW4bGohFH9ZrbASuFaU0bPqTc57jLFUmL6uzoggWG4pXlW_7-4BTXGMPscBksmAbmpkQodGwerWh86HHRpTnMCHI5gy8hl13jlIECZv-v6A4NeYIGfoUKFCTIPpjyKl-l0wYUL382CKgM95hrz0DsjNwU4-BmTKH5rmISaU5_EoFtPb6pUzfYZ3S11XP66v7i6_1bffv95cXtzWVgg-1QpIZ6V1ymCJwTLcgnLNVkkLVIiWMiOUUI4Z2dlWAZdUGetMx1lrnBCCrasvj7rF589y3qQHny30vQkQ56ybpqgRIf8Lki2meEtoAT_9A-7jnEIxoWnDCeMN5rxQH5-lqGRCsYafpHamB-2Di1My9mGvviDlLMa5wIXaPEGV18HgbQzgfPl_asCmmHMCp8fkB5MOmmD9EC2d97pESy_RKgMflmPndoDuhC9ZKsDnBTDZmt4lE6zPf3Gq2C7e19X5I5dLK-wgnVw_s_oPLG3n1g</recordid><startdate>20040708</startdate><enddate>20040708</enddate><creator>Saleem, Ahamed</creator><creator>Dutta, Jayeeta</creator><creator>Malegaonkar, Diptee</creator><creator>Rasheed, Farheena</creator><creator>Rasheed, Zeshaan</creator><creator>Rajendra, Rajeev</creator><creator>Marshall, Henderson</creator><creator>Luo, Minje</creator><creator>Li, Honghua</creator><creator>Rubin, Eric H</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>20040708</creationdate><title>The topoisomerase I- and p53-binding protein topors is differentially expressed in normal and malignant human tissues and may function as a tumor suppressor</title><author>Saleem, Ahamed ; Dutta, Jayeeta ; Malegaonkar, Diptee ; Rasheed, Farheena ; Rasheed, Zeshaan ; Rajendra, Rajeev ; Marshall, Henderson ; Luo, Minje ; Li, Honghua ; Rubin, Eric H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c554t-9e1dc7cf9a070ec30be9f6897ce255b23a5959f3a7dcb9e4729acfad43baf5553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - metabolism</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Carrier Proteins - biosynthesis</topic><topic>Cell Biology</topic><topic>Cell Cycle</topic><topic>Cell Division</topic><topic>Cell physiology</topic><topic>Cell proliferation</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Chromosome 9</topic><topic>Colon - metabolism</topic><topic>Colon cancer</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colorectal cancer</topic><topic>CpG Islands</topic><topic>Dentistry</topic><topic>DNA Methylation</topic><topic>DNA topoisomerase</topic><topic>DNA-Binding Proteins - biosynthesis</topic><topic>Flow Cytometry</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>G1 Phase</topic><topic>Gene mapping</topic><topic>Genes, Tumor Suppressor</topic><topic>Green Fluorescent Proteins</topic><topic>HeLa Cells</topic><topic>Heterozygosity</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Leukemia</topic><topic>Loss of Heterozygosity</topic><topic>Luminescent Proteins - metabolism</topic><topic>Medical schools</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular and cellular biology</topic><topic>mRNA</topic><topic>Neoplasm Proteins</topic><topic>Nuclear Proteins - biosynthesis</topic><topic>Oncology</topic><topic>original-paper</topic><topic>p53 Protein</topic><topic>Promyeloid leukemia</topic><topic>Protein Structure, Tertiary</topic><topic>Proteins</topic><topic>Resting Phase, Cell Cycle</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Thymidine - metabolism</topic><topic>Time Factors</topic><topic>Tissue Distribution</topic><topic>Transcription Factors - biosynthesis</topic><topic>Tumor cell lines</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><topic>U937 Cells</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Saleem, Ahamed</creatorcontrib><creatorcontrib>Dutta, Jayeeta</creatorcontrib><creatorcontrib>Malegaonkar, Diptee</creatorcontrib><creatorcontrib>Rasheed, Farheena</creatorcontrib><creatorcontrib>Rasheed, Zeshaan</creatorcontrib><creatorcontrib>Rajendra, Rajeev</creatorcontrib><creatorcontrib>Marshall, Henderson</creatorcontrib><creatorcontrib>Luo, Minje</creatorcontrib><creatorcontrib>Li, Honghua</creatorcontrib><creatorcontrib>Rubin, Eric 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><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>ProQuest 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>Saleem, Ahamed</au><au>Dutta, Jayeeta</au><au>Malegaonkar, Diptee</au><au>Rasheed, Farheena</au><au>Rasheed, Zeshaan</au><au>Rajendra, Rajeev</au><au>Marshall, Henderson</au><au>Luo, Minje</au><au>Li, Honghua</au><au>Rubin, Eric H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The topoisomerase I- and p53-binding protein topors is differentially expressed in normal and malignant human tissues and may function as a tumor suppressor</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2004-07-08</date><risdate>2004</risdate><volume>23</volume><issue>31</issue><spage>5293</spage><epage>5300</epage><pages>5293-5300</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Topors was identified recently as a human protein that binds to topoisomerase I and p53. Topors contains a highly conserved RING domain and localizes in promyelocytic leukemia nuclear bodies. Relatively little is known regarding topors expression patterns or function. We now demonstrate that topors mRNA and protein are widely expressed in normal human tissues. By contrast, topors mRNA and protein levels are decreased or undetectable in colon adenocarcinomas relative to normal colon tissue, and expression of the topors protein is not detectable in several colon cancer cell lines. The human
TOPORS
gene is located on chromosome 9p21, with loss of heterozygosity in this region frequently observed in several different malignancies. While we were unable to detect loss of heterozygosity of the
TOPORS
gene in 16 sporadic colon cancer cases, increased methylation of a CpG island in the
TOPORS
promoter was evident in colon adenocarcinoma specimens relative to matched normal tissues. Additional studies indicate that forced expression of topors inhibits cellular proliferation and is associated with an accumulation of cells in the G
0
/G
1
phase of the cell cycle. This effect is independent of the topors RING domain and maps to a C-terminal region of the protein. These results suggest that topors functions as a negative regulator of cell growth, and possibly as a tumor suppressor.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15107820</pmid><doi>10.1038/sj.onc.1207700</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncogene, 2004-07, Vol.23 (31), p.5293-5300 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_66689157 |
| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; SpringerLink Journals - AutoHoldings |
| subjects | Adenocarcinoma Adenocarcinoma - metabolism Apoptosis Biological and medical sciences Carrier Proteins - biosynthesis Cell Biology Cell Cycle Cell Division Cell physiology Cell proliferation Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chromosome 9 Colon - metabolism Colon cancer Colonic Neoplasms - metabolism Colorectal cancer CpG Islands Dentistry DNA Methylation DNA topoisomerase DNA-Binding Proteins - biosynthesis Flow Cytometry Fundamental and applied biological sciences. Psychology G1 Phase Gene mapping Genes, Tumor Suppressor Green Fluorescent Proteins HeLa Cells Heterozygosity Human Genetics Humans Internal Medicine Leukemia Loss of Heterozygosity Luminescent Proteins - metabolism Medical schools Medicine Medicine & Public Health Molecular and cellular biology mRNA Neoplasm Proteins Nuclear Proteins - biosynthesis Oncology original-paper p53 Protein Promyeloid leukemia Protein Structure, Tertiary Proteins Resting Phase, Cell Cycle Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Thymidine - metabolism Time Factors Tissue Distribution Transcription Factors - biosynthesis Tumor cell lines Tumor suppressor genes Tumor Suppressor Protein p53 - metabolism Tumors U937 Cells Ubiquitin-Protein Ligases - metabolism |
| title | The topoisomerase I- and p53-binding protein topors is differentially expressed in normal and malignant human tissues and may function as a tumor suppressor |
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