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CAMKK2, Regulated by Promoter Methylation, is a Prognostic Marker in Diffuse Gliomas
Summary Aims To explore the expression, methylation pattern, the prognostic value, and the biological consequences of CAMKK2 in gliomas. Methods The expression and methylation pattern of CAMKK2 was inferred and validated from mRNA expression profile (N = 866) and methylation profile (N = 426) of gli...
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Published in: | CNS neuroscience & therapeutics 2016-06, Vol.22 (6), p.518-524 |
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container_end_page | 524 |
container_issue | 6 |
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container_title | CNS neuroscience & therapeutics |
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creator | Liu, Da‐Ming Wang, Hong‐Jun Han, Bo Meng, Xiang‐Qi Chen, Ming‐Hui Yang, Dong‐Bo Sun, Ying Li, Yong‐Li Jiang, Chuan‐Lu |
description | Summary
Aims
To explore the expression, methylation pattern, the prognostic value, and the biological consequences of CAMKK2 in gliomas.
Methods
The expression and methylation pattern of CAMKK2 was inferred and validated from mRNA expression profile (N = 866) and methylation profile (N = 426) of glioma tissue samples, and independent samples were used for further validation by IHC and pyrosequencing. To explore the function of CAMKK2 in gliomas, in vitro studies, colony formation assays and migration and invasion assays were performed.
Results
We found the upregulation of CAMKK2 in high‐grade glioma samples was associated with promoter hypomethylation. An elevated expression of CAMKK2 was associated with worse prognosis. By in vitro assays, we demonstrated that CAMKK2 could promote cell migration, invasion, and proliferation.
Conclusions
The expression level of CAMKK2 could be regulated by promoter methylation. CAMKK2 serves as a prognostic marker in gliomas and could be a potential therapeutic target in gliomas. |
doi_str_mv | 10.1111/cns.12531 |
format | article |
fullrecord | <record><control><sourceid>proquest_24P</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6492904</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1789033509</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4761-850a8ec836097fe130212d3bc34924eec784e6f45ce5449e1f2c8c8e10ae14023</originalsourceid><addsrcrecordid>eNqNkV1PFDEUhhuikQ-98A-YJt5IwkI_p-2NCVk-JLBqBK6bbvfMUpyZQjsD2X9v14UNmpjYmzY9T55z2heh95Ts07IOfJf3KZOcbqAtqqQcSSPMq_WZk020nfMtIRXTRr9Bm0wRyhTnW-hqfDg5P2d7-AfMh8b1MMPTBf6eYht7SHgC_c2iXIfY7eGQsVuW5l3MffB44tLPwoQOH4W6HjLg0ybE1uW36HXtmgzvnvYddH1yfDX-Mrr4dno2PrwYeaEqOtKSOA1e84oYVQPlhFE241PPhWECwCstoKqF9CCFMEBr5rXXQIkDKgjjO-jzyns3TFuYeej65Bp7l0Lr0sJGF-yflS7c2Hl8sFVpYIgogk9PghTvB8i9bUP20DSugzhkS5UhRjAh1H-g2hDOJTEF_fgXehuH1JWfWFK6UqaSy-F3V5RPMecE9XpuSuwyVltitb9jLeyHlw9dk885FuBgBTyGBhb_Ntnx18uV8hcL3apG</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1788679652</pqid></control><display><type>article</type><title>CAMKK2, Regulated by Promoter Methylation, is a Prognostic Marker in Diffuse Gliomas</title><source>Wiley-Blackwell Titles (Open access)</source><creator>Liu, Da‐Ming ; Wang, Hong‐Jun ; Han, Bo ; Meng, Xiang‐Qi ; Chen, Ming‐Hui ; Yang, Dong‐Bo ; Sun, Ying ; Li, Yong‐Li ; Jiang, Chuan‐Lu</creator><creatorcontrib>Liu, Da‐Ming ; Wang, Hong‐Jun ; Han, Bo ; Meng, Xiang‐Qi ; Chen, Ming‐Hui ; Yang, Dong‐Bo ; Sun, Ying ; Li, Yong‐Li ; Jiang, Chuan‐Lu</creatorcontrib><description>Summary
Aims
To explore the expression, methylation pattern, the prognostic value, and the biological consequences of CAMKK2 in gliomas.
Methods
The expression and methylation pattern of CAMKK2 was inferred and validated from mRNA expression profile (N = 866) and methylation profile (N = 426) of glioma tissue samples, and independent samples were used for further validation by IHC and pyrosequencing. To explore the function of CAMKK2 in gliomas, in vitro studies, colony formation assays and migration and invasion assays were performed.
Results
We found the upregulation of CAMKK2 in high‐grade glioma samples was associated with promoter hypomethylation. An elevated expression of CAMKK2 was associated with worse prognosis. By in vitro assays, we demonstrated that CAMKK2 could promote cell migration, invasion, and proliferation.
Conclusions
The expression level of CAMKK2 could be regulated by promoter methylation. CAMKK2 serves as a prognostic marker in gliomas and could be a potential therapeutic target in gliomas.</description><identifier>ISSN: 1755-5930</identifier><identifier>EISSN: 1755-5949</identifier><identifier>DOI: 10.1111/cns.12531</identifier><identifier>PMID: 27012733</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Brain Neoplasms - diagnosis ; Brain Neoplasms - genetics ; Brain Neoplasms - mortality ; Brain Neoplasms - pathology ; Calcium-Calmodulin-Dependent Protein Kinase Kinase - genetics ; Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism ; CAMKK2 ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; DNA Methylation - genetics ; Female ; Gene Expression Regulation, Neoplastic - genetics ; Genes ; Glioma ; Glioma - diagnosis ; Glioma - genetics ; Glioma - mortality ; Glioma - pathology ; Humans ; Male ; Microarray Analysis ; Original ; Prognosis ; Progression ; Promoter Regions, Genetic ; Survival Analysis</subject><ispartof>CNS neuroscience & therapeutics, 2016-06, Vol.22 (6), p.518-524</ispartof><rights>2016 John Wiley & Sons Ltd</rights><rights>2016 John Wiley & Sons Ltd.</rights><rights>Copyright © 2016 John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4761-850a8ec836097fe130212d3bc34924eec784e6f45ce5449e1f2c8c8e10ae14023</citedby><cites>FETCH-LOGICAL-c4761-850a8ec836097fe130212d3bc34924eec784e6f45ce5449e1f2c8c8e10ae14023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6492904/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6492904/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,11561,27923,27924,46051,46475,53790,53792</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcns.12531$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27012733$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Da‐Ming</creatorcontrib><creatorcontrib>Wang, Hong‐Jun</creatorcontrib><creatorcontrib>Han, Bo</creatorcontrib><creatorcontrib>Meng, Xiang‐Qi</creatorcontrib><creatorcontrib>Chen, Ming‐Hui</creatorcontrib><creatorcontrib>Yang, Dong‐Bo</creatorcontrib><creatorcontrib>Sun, Ying</creatorcontrib><creatorcontrib>Li, Yong‐Li</creatorcontrib><creatorcontrib>Jiang, Chuan‐Lu</creatorcontrib><title>CAMKK2, Regulated by Promoter Methylation, is a Prognostic Marker in Diffuse Gliomas</title><title>CNS neuroscience & therapeutics</title><addtitle>CNS Neurosci Ther</addtitle><description>Summary
Aims
To explore the expression, methylation pattern, the prognostic value, and the biological consequences of CAMKK2 in gliomas.
Methods
The expression and methylation pattern of CAMKK2 was inferred and validated from mRNA expression profile (N = 866) and methylation profile (N = 426) of glioma tissue samples, and independent samples were used for further validation by IHC and pyrosequencing. To explore the function of CAMKK2 in gliomas, in vitro studies, colony formation assays and migration and invasion assays were performed.
Results
We found the upregulation of CAMKK2 in high‐grade glioma samples was associated with promoter hypomethylation. An elevated expression of CAMKK2 was associated with worse prognosis. By in vitro assays, we demonstrated that CAMKK2 could promote cell migration, invasion, and proliferation.
Conclusions
The expression level of CAMKK2 could be regulated by promoter methylation. CAMKK2 serves as a prognostic marker in gliomas and could be a potential therapeutic target in gliomas.</description><subject>Brain Neoplasms - diagnosis</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - mortality</subject><subject>Brain Neoplasms - pathology</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Kinase - genetics</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism</subject><subject>CAMKK2</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>DNA Methylation - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Genes</subject><subject>Glioma</subject><subject>Glioma - diagnosis</subject><subject>Glioma - genetics</subject><subject>Glioma - mortality</subject><subject>Glioma - pathology</subject><subject>Humans</subject><subject>Male</subject><subject>Microarray Analysis</subject><subject>Original</subject><subject>Prognosis</subject><subject>Progression</subject><subject>Promoter Regions, Genetic</subject><subject>Survival Analysis</subject><issn>1755-5930</issn><issn>1755-5949</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqNkV1PFDEUhhuikQ-98A-YJt5IwkI_p-2NCVk-JLBqBK6bbvfMUpyZQjsD2X9v14UNmpjYmzY9T55z2heh95Ts07IOfJf3KZOcbqAtqqQcSSPMq_WZk020nfMtIRXTRr9Bm0wRyhTnW-hqfDg5P2d7-AfMh8b1MMPTBf6eYht7SHgC_c2iXIfY7eGQsVuW5l3MffB44tLPwoQOH4W6HjLg0ybE1uW36HXtmgzvnvYddH1yfDX-Mrr4dno2PrwYeaEqOtKSOA1e84oYVQPlhFE241PPhWECwCstoKqF9CCFMEBr5rXXQIkDKgjjO-jzyns3TFuYeej65Bp7l0Lr0sJGF-yflS7c2Hl8sFVpYIgogk9PghTvB8i9bUP20DSugzhkS5UhRjAh1H-g2hDOJTEF_fgXehuH1JWfWFK6UqaSy-F3V5RPMecE9XpuSuwyVltitb9jLeyHlw9dk885FuBgBTyGBhb_Ntnx18uV8hcL3apG</recordid><startdate>201606</startdate><enddate>201606</enddate><creator>Liu, Da‐Ming</creator><creator>Wang, Hong‐Jun</creator><creator>Han, Bo</creator><creator>Meng, Xiang‐Qi</creator><creator>Chen, Ming‐Hui</creator><creator>Yang, Dong‐Bo</creator><creator>Sun, Ying</creator><creator>Li, Yong‐Li</creator><creator>Jiang, Chuan‐Lu</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><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>7TK</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201606</creationdate><title>CAMKK2, Regulated by Promoter Methylation, is a Prognostic Marker in Diffuse Gliomas</title><author>Liu, Da‐Ming ; Wang, Hong‐Jun ; Han, Bo ; Meng, Xiang‐Qi ; Chen, Ming‐Hui ; Yang, Dong‐Bo ; Sun, Ying ; Li, Yong‐Li ; Jiang, Chuan‐Lu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4761-850a8ec836097fe130212d3bc34924eec784e6f45ce5449e1f2c8c8e10ae14023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Brain Neoplasms - diagnosis</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - mortality</topic><topic>Brain Neoplasms - pathology</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Kinase - genetics</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism</topic><topic>CAMKK2</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>DNA Methylation - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Genes</topic><topic>Glioma</topic><topic>Glioma - diagnosis</topic><topic>Glioma - genetics</topic><topic>Glioma - mortality</topic><topic>Glioma - pathology</topic><topic>Humans</topic><topic>Male</topic><topic>Microarray Analysis</topic><topic>Original</topic><topic>Prognosis</topic><topic>Progression</topic><topic>Promoter Regions, Genetic</topic><topic>Survival Analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Da‐Ming</creatorcontrib><creatorcontrib>Wang, Hong‐Jun</creatorcontrib><creatorcontrib>Han, Bo</creatorcontrib><creatorcontrib>Meng, Xiang‐Qi</creatorcontrib><creatorcontrib>Chen, Ming‐Hui</creatorcontrib><creatorcontrib>Yang, Dong‐Bo</creatorcontrib><creatorcontrib>Sun, Ying</creatorcontrib><creatorcontrib>Li, Yong‐Li</creatorcontrib><creatorcontrib>Jiang, Chuan‐Lu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>CNS neuroscience & therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Liu, Da‐Ming</au><au>Wang, Hong‐Jun</au><au>Han, Bo</au><au>Meng, Xiang‐Qi</au><au>Chen, Ming‐Hui</au><au>Yang, Dong‐Bo</au><au>Sun, Ying</au><au>Li, Yong‐Li</au><au>Jiang, Chuan‐Lu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CAMKK2, Regulated by Promoter Methylation, is a Prognostic Marker in Diffuse Gliomas</atitle><jtitle>CNS neuroscience & therapeutics</jtitle><addtitle>CNS Neurosci Ther</addtitle><date>2016-06</date><risdate>2016</risdate><volume>22</volume><issue>6</issue><spage>518</spage><epage>524</epage><pages>518-524</pages><issn>1755-5930</issn><eissn>1755-5949</eissn><abstract>Summary
Aims
To explore the expression, methylation pattern, the prognostic value, and the biological consequences of CAMKK2 in gliomas.
Methods
The expression and methylation pattern of CAMKK2 was inferred and validated from mRNA expression profile (N = 866) and methylation profile (N = 426) of glioma tissue samples, and independent samples were used for further validation by IHC and pyrosequencing. To explore the function of CAMKK2 in gliomas, in vitro studies, colony formation assays and migration and invasion assays were performed.
Results
We found the upregulation of CAMKK2 in high‐grade glioma samples was associated with promoter hypomethylation. An elevated expression of CAMKK2 was associated with worse prognosis. By in vitro assays, we demonstrated that CAMKK2 could promote cell migration, invasion, and proliferation.
Conclusions
The expression level of CAMKK2 could be regulated by promoter methylation. CAMKK2 serves as a prognostic marker in gliomas and could be a potential therapeutic target in gliomas.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>27012733</pmid><doi>10.1111/cns.12531</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Brain Neoplasms - diagnosis Brain Neoplasms - genetics Brain Neoplasms - mortality Brain Neoplasms - pathology Calcium-Calmodulin-Dependent Protein Kinase Kinase - genetics Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism CAMKK2 Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics DNA Methylation - genetics Female Gene Expression Regulation, Neoplastic - genetics Genes Glioma Glioma - diagnosis Glioma - genetics Glioma - mortality Glioma - pathology Humans Male Microarray Analysis Original Prognosis Progression Promoter Regions, Genetic Survival Analysis |
title | CAMKK2, Regulated by Promoter Methylation, is a Prognostic Marker in Diffuse Gliomas |
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