CT120 : A New Potential Target for c-Myc in Head and Neck Cancers
: CT120 is a universally expressed protein with seven transmembrane domains. It functions in cell proliferation, survival and apoptosis by activating Raf/MEK/ERK and PI3K/Akt signaling pathways. Evidence suggests that CT120 plays important roles in lung carcinogenesis and oncogenic pathway activatio...
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Veröffentlicht in: | Journal of Cancer 2017-01, Vol.8 (5), p.880-886 |
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creator | Baltaci, Elif Seyhan, Betül Baykara, Onur Buyru, Nur |
description | : CT120 is a universally expressed protein with seven transmembrane domains. It functions in cell proliferation, survival and apoptosis by activating Raf/MEK/ERK and PI3K/Akt signaling pathways. Evidence suggests that CT120 plays important roles in lung carcinogenesis and oncogenic pathway activation. c-Myc is an important transcription factor modulating cell progression, apoptosis and cellular transformation. Previous studies have shown that
gene is amplified in many types of cancer including head and neck squamous cell carcinoma (HNSCC). Myc can regulate expression of many genes by binding to E-boxes. The aim of this study was to investigate the relationship between c-Myc protein and
gene.
Tumor and normal tissue samples from 50 patients with HNSCC were investigated with chromatin immunoprecipitation assay (ChIP), Illumina MiSeq, bisulphite sequencing and qRT-PCR.
c-Myc binds to all E-boxes except E-box 5 on
promoter. The CpG dinucleotides were found to be partially methylated in all tumor and normal tissue samples. Bisulphite sequencing showed a 10% down-regulation in the methylation levels of the tumor tissues.
gene was hypomethylated and up-regulated in 56% of the tumor tissue samples. Expression of c-Myc was significantly higher in tumor tissues than in non-cancerous tissue samples.
was overexpressed in 68% of the tumor tissue samples compared to normal tissues. The mean
levels were 2.42-fold higher in the tumor tissue samples. In 48% of the tumor tissues,
and
mRNA were up- or down-regulated simultaneously (p |
doi_str_mv | 10.7150/jca.18207 |
format | Article |
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gene is amplified in many types of cancer including head and neck squamous cell carcinoma (HNSCC). Myc can regulate expression of many genes by binding to E-boxes. The aim of this study was to investigate the relationship between c-Myc protein and
gene.
Tumor and normal tissue samples from 50 patients with HNSCC were investigated with chromatin immunoprecipitation assay (ChIP), Illumina MiSeq, bisulphite sequencing and qRT-PCR.
c-Myc binds to all E-boxes except E-box 5 on
promoter. The CpG dinucleotides were found to be partially methylated in all tumor and normal tissue samples. Bisulphite sequencing showed a 10% down-regulation in the methylation levels of the tumor tissues.
gene was hypomethylated and up-regulated in 56% of the tumor tissue samples. Expression of c-Myc was significantly higher in tumor tissues than in non-cancerous tissue samples.
was overexpressed in 68% of the tumor tissue samples compared to normal tissues. The mean
levels were 2.42-fold higher in the tumor tissue samples. In 48% of the tumor tissues,
and
mRNA were up- or down-regulated simultaneously (p<0.001).
We show that
gene is a target of c-Myc and it contributes to cancer progression in HNSCC.</description><identifier>ISSN: 1837-9664</identifier><identifier>EISSN: 1837-9664</identifier><identifier>DOI: 10.7150/jca.18207</identifier><identifier>PMID: 28382151</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher</publisher><subject>Research Paper</subject><ispartof>Journal of Cancer, 2017-01, Vol.8 (5), p.880-886</ispartof><rights>Ivyspring International Publisher 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-88f5f2260014090a50df1fb6d2c5283cbf8ff42a7686a421544d2e97258338993</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381177/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381177/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28382151$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Baltaci, Elif</creatorcontrib><creatorcontrib>Seyhan, Betül</creatorcontrib><creatorcontrib>Baykara, Onur</creatorcontrib><creatorcontrib>Buyru, Nur</creatorcontrib><title>CT120 : A New Potential Target for c-Myc in Head and Neck Cancers</title><title>Journal of Cancer</title><addtitle>J Cancer</addtitle><description>: CT120 is a universally expressed protein with seven transmembrane domains. It functions in cell proliferation, survival and apoptosis by activating Raf/MEK/ERK and PI3K/Akt signaling pathways. Evidence suggests that CT120 plays important roles in lung carcinogenesis and oncogenic pathway activation. c-Myc is an important transcription factor modulating cell progression, apoptosis and cellular transformation. Previous studies have shown that
gene is amplified in many types of cancer including head and neck squamous cell carcinoma (HNSCC). Myc can regulate expression of many genes by binding to E-boxes. The aim of this study was to investigate the relationship between c-Myc protein and
gene.
Tumor and normal tissue samples from 50 patients with HNSCC were investigated with chromatin immunoprecipitation assay (ChIP), Illumina MiSeq, bisulphite sequencing and qRT-PCR.
c-Myc binds to all E-boxes except E-box 5 on
promoter. The CpG dinucleotides were found to be partially methylated in all tumor and normal tissue samples. Bisulphite sequencing showed a 10% down-regulation in the methylation levels of the tumor tissues.
gene was hypomethylated and up-regulated in 56% of the tumor tissue samples. Expression of c-Myc was significantly higher in tumor tissues than in non-cancerous tissue samples.
was overexpressed in 68% of the tumor tissue samples compared to normal tissues. The mean
levels were 2.42-fold higher in the tumor tissue samples. In 48% of the tumor tissues,
and
mRNA were up- or down-regulated simultaneously (p<0.001).
We show that
gene is a target of c-Myc and it contributes to cancer progression in HNSCC.</description><subject>Research Paper</subject><issn>1837-9664</issn><issn>1837-9664</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNpVkE1PAjEURRujEYIs_AOmS10M9nPacWFCJiom-LHAdVM6LQ4OM9gOGP69VZBgN6_JO7nv5AJwjtFAYI6u50YPsCRIHIEullQkWZqy44N_B_RDmKP4aEYEo6egQySVBHPcBcN8ggmCN3AIn-0XfG1aW7elruBE-5ltoWs8NMnTxsCyhiOrC6jrIqLmA-a6NtaHM3DidBVsfzd74O3-bpKPkvHLw2M-HCeGCt4mUjruCEkRwgxlSHNUOOymaUEMjzpm6qRzjGiRylSzKMdYQWwmCJeUyiyjPXC7zV2upgtbmOjpdaWWvlxov1GNLtX_TV2-q1mzVpxKjIWIAZe7AN98rmxo1aIMxlaVrm2zCgpLyWSGiSQRvdqixjcheOv2ZzBSP62r2Lr6bT2yF4dee_KvY_oNHb15aA</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Baltaci, Elif</creator><creator>Seyhan, Betül</creator><creator>Baykara, Onur</creator><creator>Buyru, Nur</creator><general>Ivyspring International Publisher</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170101</creationdate><title>CT120 : A New Potential Target for c-Myc in Head and Neck Cancers</title><author>Baltaci, Elif ; Seyhan, Betül ; Baykara, Onur ; Buyru, Nur</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-88f5f2260014090a50df1fb6d2c5283cbf8ff42a7686a421544d2e97258338993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Research Paper</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Baltaci, Elif</creatorcontrib><creatorcontrib>Seyhan, Betül</creatorcontrib><creatorcontrib>Baykara, Onur</creatorcontrib><creatorcontrib>Buyru, Nur</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baltaci, Elif</au><au>Seyhan, Betül</au><au>Baykara, Onur</au><au>Buyru, Nur</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CT120 : A New Potential Target for c-Myc in Head and Neck Cancers</atitle><jtitle>Journal of Cancer</jtitle><addtitle>J Cancer</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>8</volume><issue>5</issue><spage>880</spage><epage>886</epage><pages>880-886</pages><issn>1837-9664</issn><eissn>1837-9664</eissn><abstract>: CT120 is a universally expressed protein with seven transmembrane domains. It functions in cell proliferation, survival and apoptosis by activating Raf/MEK/ERK and PI3K/Akt signaling pathways. Evidence suggests that CT120 plays important roles in lung carcinogenesis and oncogenic pathway activation. c-Myc is an important transcription factor modulating cell progression, apoptosis and cellular transformation. Previous studies have shown that
gene is amplified in many types of cancer including head and neck squamous cell carcinoma (HNSCC). Myc can regulate expression of many genes by binding to E-boxes. The aim of this study was to investigate the relationship between c-Myc protein and
gene.
Tumor and normal tissue samples from 50 patients with HNSCC were investigated with chromatin immunoprecipitation assay (ChIP), Illumina MiSeq, bisulphite sequencing and qRT-PCR.
c-Myc binds to all E-boxes except E-box 5 on
promoter. The CpG dinucleotides were found to be partially methylated in all tumor and normal tissue samples. Bisulphite sequencing showed a 10% down-regulation in the methylation levels of the tumor tissues.
gene was hypomethylated and up-regulated in 56% of the tumor tissue samples. Expression of c-Myc was significantly higher in tumor tissues than in non-cancerous tissue samples.
was overexpressed in 68% of the tumor tissue samples compared to normal tissues. The mean
levels were 2.42-fold higher in the tumor tissue samples. In 48% of the tumor tissues,
and
mRNA were up- or down-regulated simultaneously (p<0.001).
We show that
gene is a target of c-Myc and it contributes to cancer progression in HNSCC.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher</pub><pmid>28382151</pmid><doi>10.7150/jca.18207</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Research Paper |
title | CT120 : A New Potential Target for c-Myc in Head and Neck Cancers |
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