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Biphasic regulation of tumorigenesis by PTK7 expression level in esophageal squamous cell carcinoma
Protein tyrosine kinase 7 (PTK7), also known as colon carcinoma kinase 4 (CCK-4), is a member of the catalytically defective receptor protein tyrosine kinase family and is upregulated in various cancers, where it is known to act as either an oncoprotein or a tumor suppressor. To understand the contr...
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Published in: | Scientific reports 2018-06, Vol.8 (1), p.8519-9, Article 8519 |
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description | Protein tyrosine kinase 7 (PTK7), also known as colon carcinoma kinase 4 (CCK-4), is a member of the catalytically defective receptor protein tyrosine kinase family and is upregulated in various cancers, where it is known to act as either an oncoprotein or a tumor suppressor. To understand the contrasting roles of PTK7 in tumorigenesis, we analyzed the tumorigenic characteristics of esophageal squamous cell carcinoma (ESCC) cells with low levels of endogenous PTK7 expression (TE-5 and TE-14 cells) and high levels of expression (TE-6 and TE-10 cells) after transfections with a PTK7 expression vector. PTK7 overexpression increased the proliferation of TE-5 and TE-14 cells but decreased the proliferation of TE-6 and TE-10 cells. In the ESCC cells, proliferation, migration, and invasion were initially increased and then decreased according to PTK7 expression levels, which were mirrored by initial increases and then decreases in the tyrosine phosphorylation of cellular proteins and phosphorylation of Src, Akt, and ERK. In ESCC patients included in The Cancer Genome Atlas database, those with higher PTK7 mRNA levels had a longer overall survival and lower relative risk than those with lower PTK7 mRNA levels. These results demonstrate that PTK7 biphasically regulates tumorigenesis in ESCC. |
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To understand the contrasting roles of PTK7 in tumorigenesis, we analyzed the tumorigenic characteristics of esophageal squamous cell carcinoma (ESCC) cells with low levels of endogenous PTK7 expression (TE-5 and TE-14 cells) and high levels of expression (TE-6 and TE-10 cells) after transfections with a PTK7 expression vector. PTK7 overexpression increased the proliferation of TE-5 and TE-14 cells but decreased the proliferation of TE-6 and TE-10 cells. In the ESCC cells, proliferation, migration, and invasion were initially increased and then decreased according to PTK7 expression levels, which were mirrored by initial increases and then decreases in the tyrosine phosphorylation of cellular proteins and phosphorylation of Src, Akt, and ERK. In ESCC patients included in The Cancer Genome Atlas database, those with higher PTK7 mRNA levels had a longer overall survival and lower relative risk than those with lower PTK7 mRNA levels. These results demonstrate that PTK7 biphasically regulates tumorigenesis in ESCC.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-26957-6</identifier><identifier>PMID: 29867084</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>AKT protein ; Cell migration ; Cell proliferation ; Cholecystokinin ; Colon ; Esophageal cancer ; Esophagus ; Extracellular signal-regulated kinase ; Genomes ; Kinases ; mRNA ; Phosphorylation ; Protein-tyrosine kinase ; Squamous cell carcinoma ; Tumor suppressor genes ; Tumorigenesis</subject><ispartof>Scientific reports, 2018-06, Vol.8 (1), p.8519-9, Article 8519</ispartof><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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Gim, Jungsoo ; Won, Sungho ; Lee, Seung-Taek</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c467t-d9049eef00c64d0146b397609717897bc1fc9346fd5d37aa438cc57b0c7128683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>AKT protein</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Cholecystokinin</topic><topic>Colon</topic><topic>Esophageal cancer</topic><topic>Esophagus</topic><topic>Extracellular signal-regulated kinase</topic><topic>Genomes</topic><topic>Kinases</topic><topic>mRNA</topic><topic>Phosphorylation</topic><topic>Protein-tyrosine kinase</topic><topic>Squamous cell carcinoma</topic><topic>Tumor suppressor genes</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shin, Won-Sik</creatorcontrib><creatorcontrib>Gim, Jungsoo</creatorcontrib><creatorcontrib>Won, Sungho</creatorcontrib><creatorcontrib>Lee, Seung-Taek</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</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>Science Database (Alumni Edition)</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>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>PML(ProQuest Medical Library)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shin, Won-Sik</au><au>Gim, Jungsoo</au><au>Won, Sungho</au><au>Lee, Seung-Taek</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biphasic regulation of tumorigenesis by PTK7 expression level in esophageal squamous cell carcinoma</atitle><jtitle>Scientific reports</jtitle><addtitle>Sci Rep</addtitle><date>2018-06-04</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>8519</spage><epage>9</epage><pages>8519-9</pages><artnum>8519</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Protein tyrosine kinase 7 (PTK7), also known as colon carcinoma kinase 4 (CCK-4), is a member of the catalytically defective receptor protein tyrosine kinase family and is upregulated in various cancers, where it is known to act as either an oncoprotein or a tumor suppressor. 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subjects | AKT protein Cell migration Cell proliferation Cholecystokinin Colon Esophageal cancer Esophagus Extracellular signal-regulated kinase Genomes Kinases mRNA Phosphorylation Protein-tyrosine kinase Squamous cell carcinoma Tumor suppressor genes Tumorigenesis |
title | Biphasic regulation of tumorigenesis by PTK7 expression level in esophageal squamous cell carcinoma |
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