5-aza-CdR induces the demethylation of Syk promoter in nasopharyngeal carcinoma cell
The present study employed 5-aza-2′-deoxycytidine (5-aza-CdR) to treat nasopharyngeal carcinoma cell line CNE-1, CNE-2 and non-cancerous human nasopharyngeal epithelial cell line NP-69 to understand the effects on spleen tyrosine kinase (Syk) gene promoter methylation. The results showed that the me...
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| Veröffentlicht in: | Gene 2012-12, Vol.511 (2), p.224-226 |
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| creator | Jin, Qiaozhi Liu, Chibo Yan, Chong Tao, Baohong Li, Zhihai Cai, Zhiyi |
| description | The present study employed 5-aza-2′-deoxycytidine (5-aza-CdR) to treat nasopharyngeal carcinoma cell line CNE-1, CNE-2 and non-cancerous human nasopharyngeal epithelial cell line NP-69 to understand the effects on spleen tyrosine kinase (Syk) gene promoter methylation. The results showed that the methylation level of Syk gene is negatively associated with the differentiation level of the cell lines, and the 5-aza-CdR treatment decreased the methylation level in nasopharyngeal carcinoma cell lines. Additionally, the drug sensitivity of low-differentiated cell line was significantly higher than the high-differentiated cell line. In conclusion, the Syk gene promoter methylation reflects the cell differentiation status, and 5-aza-CdR treatment could induce the demethylation of Syk gene promoter.
► 5-aza-2'-deoxycytidine (5-aza-CdR) was used to treat nasopharyngeal carcinoma cells. ► The study looked at the Syk gene promoter methylation after the treatment. ► In nasopharyngeal carcinoma cell lines, the methylation status is high. ► This decreased the promoter methylation and increased the Syk gene expression. |
| doi_str_mv | 10.1016/j.gene.2012.09.053 |
| format | Article |
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► 5-aza-2'-deoxycytidine (5-aza-CdR) was used to treat nasopharyngeal carcinoma cells. ► The study looked at the Syk gene promoter methylation after the treatment. ► In nasopharyngeal carcinoma cell lines, the methylation status is high. ► This decreased the promoter methylation and increased the Syk gene expression.</description><identifier>ISSN: 0378-1119</identifier><identifier>EISSN: 1879-0038</identifier><identifier>DOI: 10.1016/j.gene.2012.09.053</identifier><identifier>PMID: 23036706</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>5-aza-2'-deoxycytidine ; 5-aza-CdR ; Antimetabolites, Antineoplastic - pharmacology ; Azacitidine - analogs & derivatives ; Azacitidine - pharmacology ; Base Sequence ; Blotting, Western ; carcinoma ; cell differentiation ; Cell Line, Tumor ; Demethylation ; Differentiation ; DNA Methylation ; DNA Primers ; Drugs ; Epithelial cells ; genes ; Humans ; Intracellular Signaling Peptides and Proteins - genetics ; methylation ; Nasopharyngeal carcinoma ; Nasopharyngeal Neoplasms - genetics ; Nasopharyngeal Neoplasms - pathology ; Promoter Regions, Genetic ; Promoters ; Protein-tyrosine kinase ; Protein-Tyrosine Kinases - genetics ; Real-Time Polymerase Chain Reaction ; RNA, Messenger - genetics ; Spleen ; Syk ; Syk Kinase ; Syk protein ; Tumor cell lines</subject><ispartof>Gene, 2012-12, Vol.511 (2), p.224-226</ispartof><rights>2012 Elsevier B.V.</rights><rights>Copyright © 2012 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-2b1c735e0f68110d199b38216d7203397a61edf5e596345f2d862258c33523213</citedby><cites>FETCH-LOGICAL-c413t-2b1c735e0f68110d199b38216d7203397a61edf5e596345f2d862258c33523213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.gene.2012.09.053$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23036706$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jin, Qiaozhi</creatorcontrib><creatorcontrib>Liu, Chibo</creatorcontrib><creatorcontrib>Yan, Chong</creatorcontrib><creatorcontrib>Tao, Baohong</creatorcontrib><creatorcontrib>Li, Zhihai</creatorcontrib><creatorcontrib>Cai, Zhiyi</creatorcontrib><title>5-aza-CdR induces the demethylation of Syk promoter in nasopharyngeal carcinoma cell</title><title>Gene</title><addtitle>Gene</addtitle><description>The present study employed 5-aza-2′-deoxycytidine (5-aza-CdR) to treat nasopharyngeal carcinoma cell line CNE-1, CNE-2 and non-cancerous human nasopharyngeal epithelial cell line NP-69 to understand the effects on spleen tyrosine kinase (Syk) gene promoter methylation. The results showed that the methylation level of Syk gene is negatively associated with the differentiation level of the cell lines, and the 5-aza-CdR treatment decreased the methylation level in nasopharyngeal carcinoma cell lines. Additionally, the drug sensitivity of low-differentiated cell line was significantly higher than the high-differentiated cell line. In conclusion, the Syk gene promoter methylation reflects the cell differentiation status, and 5-aza-CdR treatment could induce the demethylation of Syk gene promoter.
► 5-aza-2'-deoxycytidine (5-aza-CdR) was used to treat nasopharyngeal carcinoma cells. ► The study looked at the Syk gene promoter methylation after the treatment. ► In nasopharyngeal carcinoma cell lines, the methylation status is high. ► This decreased the promoter methylation and increased the Syk gene expression.</description><subject>5-aza-2'-deoxycytidine</subject><subject>5-aza-CdR</subject><subject>Antimetabolites, Antineoplastic - pharmacology</subject><subject>Azacitidine - analogs & derivatives</subject><subject>Azacitidine - pharmacology</subject><subject>Base Sequence</subject><subject>Blotting, Western</subject><subject>carcinoma</subject><subject>cell differentiation</subject><subject>Cell Line, Tumor</subject><subject>Demethylation</subject><subject>Differentiation</subject><subject>DNA Methylation</subject><subject>DNA Primers</subject><subject>Drugs</subject><subject>Epithelial cells</subject><subject>genes</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>methylation</subject><subject>Nasopharyngeal carcinoma</subject><subject>Nasopharyngeal Neoplasms - genetics</subject><subject>Nasopharyngeal Neoplasms - pathology</subject><subject>Promoter Regions, Genetic</subject><subject>Promoters</subject><subject>Protein-tyrosine kinase</subject><subject>Protein-Tyrosine Kinases - genetics</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Spleen</subject><subject>Syk</subject><subject>Syk Kinase</subject><subject>Syk protein</subject><subject>Tumor cell lines</subject><issn>0378-1119</issn><issn>1879-0038</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc2OFCEURonROO3oC7hQlm6q5EJDQeLGdPxLJjFxZtaEhlvdtFVFC9Um7dNLpUeXRhawOffLdw-EvATWAgP19tDucMKWM-AtMy2T4hFZge5Mw5jQj8mKiU43AGCuyLNSDqweKflTcsUFE6pjakXuZON-uWYTvtE4hZPHQuc90oAjzvvz4OaYJpp6env-To85jWnGXEk6uZKOe5fP0w7dQL3LPk5pdNTjMDwnT3o3FHzx8F6T-48f7jafm5uvn75s3t80fg1ibvgWfCcksl5pABbAmK3QHFToOBPCdE4Bhl6iNEqsZc-DVpxL7YWQXHAQ1-TNJbc2-3HCMtsxlqWAmzCdigXoQBtZ7_9AuVIcuNEV5RfU51RKxt4ecxzrqhaYXcTbg13E20W8ZcZW8XXo1UP-aTti-Dvyx3QFXl-A3iXrdjkWe39bE2T9lLXQeiHeXQisyn5GzLb4iJPHEDP62YYU_9XgN-gNmsQ</recordid><startdate>20121215</startdate><enddate>20121215</enddate><creator>Jin, Qiaozhi</creator><creator>Liu, Chibo</creator><creator>Yan, Chong</creator><creator>Tao, Baohong</creator><creator>Li, Zhihai</creator><creator>Cai, Zhiyi</creator><general>Elsevier B.V</general><scope>FBQ</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>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20121215</creationdate><title>5-aza-CdR induces the demethylation of Syk promoter in nasopharyngeal carcinoma cell</title><author>Jin, Qiaozhi ; Liu, Chibo ; Yan, Chong ; Tao, Baohong ; Li, Zhihai ; Cai, Zhiyi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-2b1c735e0f68110d199b38216d7203397a61edf5e596345f2d862258c33523213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>5-aza-2'-deoxycytidine</topic><topic>5-aza-CdR</topic><topic>Antimetabolites, Antineoplastic - pharmacology</topic><topic>Azacitidine - analogs & derivatives</topic><topic>Azacitidine - pharmacology</topic><topic>Base Sequence</topic><topic>Blotting, Western</topic><topic>carcinoma</topic><topic>cell differentiation</topic><topic>Cell Line, Tumor</topic><topic>Demethylation</topic><topic>Differentiation</topic><topic>DNA Methylation</topic><topic>DNA Primers</topic><topic>Drugs</topic><topic>Epithelial cells</topic><topic>genes</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>methylation</topic><topic>Nasopharyngeal carcinoma</topic><topic>Nasopharyngeal Neoplasms - genetics</topic><topic>Nasopharyngeal Neoplasms - pathology</topic><topic>Promoter Regions, Genetic</topic><topic>Promoters</topic><topic>Protein-tyrosine kinase</topic><topic>Protein-Tyrosine Kinases - genetics</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Spleen</topic><topic>Syk</topic><topic>Syk Kinase</topic><topic>Syk protein</topic><topic>Tumor cell lines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jin, Qiaozhi</creatorcontrib><creatorcontrib>Liu, Chibo</creatorcontrib><creatorcontrib>Yan, Chong</creatorcontrib><creatorcontrib>Tao, Baohong</creatorcontrib><creatorcontrib>Li, Zhihai</creatorcontrib><creatorcontrib>Cai, Zhiyi</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Gene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jin, Qiaozhi</au><au>Liu, Chibo</au><au>Yan, Chong</au><au>Tao, Baohong</au><au>Li, Zhihai</au><au>Cai, Zhiyi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>5-aza-CdR induces the demethylation of Syk promoter in nasopharyngeal carcinoma cell</atitle><jtitle>Gene</jtitle><addtitle>Gene</addtitle><date>2012-12-15</date><risdate>2012</risdate><volume>511</volume><issue>2</issue><spage>224</spage><epage>226</epage><pages>224-226</pages><issn>0378-1119</issn><eissn>1879-0038</eissn><abstract>The present study employed 5-aza-2′-deoxycytidine (5-aza-CdR) to treat nasopharyngeal carcinoma cell line CNE-1, CNE-2 and non-cancerous human nasopharyngeal epithelial cell line NP-69 to understand the effects on spleen tyrosine kinase (Syk) gene promoter methylation. The results showed that the methylation level of Syk gene is negatively associated with the differentiation level of the cell lines, and the 5-aza-CdR treatment decreased the methylation level in nasopharyngeal carcinoma cell lines. Additionally, the drug sensitivity of low-differentiated cell line was significantly higher than the high-differentiated cell line. In conclusion, the Syk gene promoter methylation reflects the cell differentiation status, and 5-aza-CdR treatment could induce the demethylation of Syk gene promoter.
► 5-aza-2'-deoxycytidine (5-aza-CdR) was used to treat nasopharyngeal carcinoma cells. ► The study looked at the Syk gene promoter methylation after the treatment. ► In nasopharyngeal carcinoma cell lines, the methylation status is high. ► This decreased the promoter methylation and increased the Syk gene expression.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>23036706</pmid><doi>10.1016/j.gene.2012.09.053</doi><tpages>3</tpages></addata></record> |
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| subjects | 5-aza-2'-deoxycytidine 5-aza-CdR Antimetabolites, Antineoplastic - pharmacology Azacitidine - analogs & derivatives Azacitidine - pharmacology Base Sequence Blotting, Western carcinoma cell differentiation Cell Line, Tumor Demethylation Differentiation DNA Methylation DNA Primers Drugs Epithelial cells genes Humans Intracellular Signaling Peptides and Proteins - genetics methylation Nasopharyngeal carcinoma Nasopharyngeal Neoplasms - genetics Nasopharyngeal Neoplasms - pathology Promoter Regions, Genetic Promoters Protein-tyrosine kinase Protein-Tyrosine Kinases - genetics Real-Time Polymerase Chain Reaction RNA, Messenger - genetics Spleen Syk Syk Kinase Syk protein Tumor cell lines |
| title | 5-aza-CdR induces the demethylation of Syk promoter in nasopharyngeal carcinoma cell |
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