Deregulation of Aurora kinase gene expression in human testicular germ cell tumours

Summary The Aurora kinases regulate chromosome segregation and cytokinesis, and alterations in their expression associate with cell malignant transformation. In this study, we demonstrated by qRT‐PCR analysis of 14 seminomas that Aurora‐A mRNA was, with respect to control tissues, augmented in five...

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Veröffentlicht in:Andrologia 2010-08, Vol.42 (4), p.260-267
Hauptverfasser: Baldini, E., Arlot-Bonnemains, Y., Mottolese, M., Sentinelli, S., Antoniani, B., Sorrenti, S., Salducci, M., Comini, E., Ulisse, S., D'Armiento, M.
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container_issue 4
container_start_page 260
container_title Andrologia
container_volume 42
creator Baldini, E.
Arlot-Bonnemains, Y.
Mottolese, M.
Sentinelli, S.
Antoniani, B.
Sorrenti, S.
Salducci, M.
Comini, E.
Ulisse, S.
D'Armiento, M.
description Summary The Aurora kinases regulate chromosome segregation and cytokinesis, and alterations in their expression associate with cell malignant transformation. In this study, we demonstrated by qRT‐PCR analysis of 14 seminomas that Aurora‐A mRNA was, with respect to control tissues, augmented in five of 14 tumour tissues by 2.17 ± 0.30 fold (P 
doi_str_mv 10.1111/j.1439-0272.2009.00987.x
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In this study, we demonstrated by qRT‐PCR analysis of 14 seminomas that Aurora‐A mRNA was, with respect to control tissues, augmented in five of 14 tumour tissues by 2.17 ± 0.30 fold (P < 0.05) and reduced in 9 to 0.38 ± 0.10 (P < 0.01). Aurora‐B mRNA was increased in 11 tumour tissues by 4.33 ± 0.82 fold (P < 0.01) and reduced in 3 to 0.41 ± 0.11 fold. Aurora‐C mRNA was reduced to 0.20 ± 0.32 fold (P < 0.01) in 13 seminomas and up‐regulated in one case. Western blot experiments, performed on protein extracts of nine seminomas and six normal testes, showed an up‐regulation of Aurora‐B protein by 10.14 ± 3.51 fold (P < 0.05), while Aurora‐A protein was found increased in four seminomas by 2.16 ± 0.43 (P < 0.05), unchanged in three and reduced in two tumour tissues. Aurora‐C protein was increased by 9.2 ± 2.90 fold (P < 0.05), suggesting that post‐transcriptional mechanisms modulate its expression. In conclusion, we demonstrated that expression of Aurora kinases is deregulated in seminomas, suggesting that they may play a role in the progression of testicular cancers.]]></description><identifier>ISSN: 0303-4569</identifier><identifier>EISSN: 1439-0272</identifier><identifier>DOI: 10.1111/j.1439-0272.2009.00987.x</identifier><identifier>PMID: 20629650</identifier><identifier>CODEN: ANDRDQ</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Aneuploidy ; Aurora Kinase B ; Aurora Kinase C ; Aurora Kinases ; Biological and medical sciences ; Cancer ; Cellular Biology ; Chromosome aberrations ; Gene Expression Regulation, Neoplastic ; genomic instability ; Gynecology. Andrology. Obstetrics ; Humans ; Life Sciences ; Male ; Male genital diseases ; Medical genetics ; Medical sciences ; Middle Aged ; mitosis ; Neoplasms, Germ Cell and Embryonal - genetics ; Protein-Serine-Threonine Kinases - genetics ; RNA, Messenger ; Seminoma - genetics ; testicular germ cell tumour ; Testicular Neoplasms - genetics ; Testis - enzymology ; Up-Regulation</subject><ispartof>Andrologia, 2010-08, Vol.42 (4), p.260-267</ispartof><rights>2010 Blackwell Verlag GmbH</rights><rights>2015 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4737-b5a3d1e1d0d33fbf918d81557fe67e7551b5d6e5203e435763b1f63f753b74ac3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1439-0272.2009.00987.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1439-0272.2009.00987.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,782,786,887,1419,27933,27934,45583,45584</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=23005095$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20629650$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://inserm.hal.science/inserm-00511226$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Baldini, E.</creatorcontrib><creatorcontrib>Arlot-Bonnemains, Y.</creatorcontrib><creatorcontrib>Mottolese, M.</creatorcontrib><creatorcontrib>Sentinelli, S.</creatorcontrib><creatorcontrib>Antoniani, B.</creatorcontrib><creatorcontrib>Sorrenti, S.</creatorcontrib><creatorcontrib>Salducci, M.</creatorcontrib><creatorcontrib>Comini, E.</creatorcontrib><creatorcontrib>Ulisse, S.</creatorcontrib><creatorcontrib>D'Armiento, M.</creatorcontrib><title>Deregulation of Aurora kinase gene expression in human testicular germ cell tumours</title><title>Andrologia</title><addtitle>Andrologia</addtitle><description><![CDATA[Summary The Aurora kinases regulate chromosome segregation and cytokinesis, and alterations in their expression associate with cell malignant transformation. In this study, we demonstrated by qRT‐PCR analysis of 14 seminomas that Aurora‐A mRNA was, with respect to control tissues, augmented in five of 14 tumour tissues by 2.17 ± 0.30 fold (P < 0.05) and reduced in 9 to 0.38 ± 0.10 (P < 0.01). Aurora‐B mRNA was increased in 11 tumour tissues by 4.33 ± 0.82 fold (P < 0.01) and reduced in 3 to 0.41 ± 0.11 fold. Aurora‐C mRNA was reduced to 0.20 ± 0.32 fold (P < 0.01) in 13 seminomas and up‐regulated in one case. Western blot experiments, performed on protein extracts of nine seminomas and six normal testes, showed an up‐regulation of Aurora‐B protein by 10.14 ± 3.51 fold (P < 0.05), while Aurora‐A protein was found increased in four seminomas by 2.16 ± 0.43 (P < 0.05), unchanged in three and reduced in two tumour tissues. Aurora‐C protein was increased by 9.2 ± 2.90 fold (P < 0.05), suggesting that post‐transcriptional mechanisms modulate its expression. In conclusion, we demonstrated that expression of Aurora kinases is deregulated in seminomas, suggesting that they may play a role in the progression of testicular cancers.]]></description><subject>Adult</subject><subject>Aneuploidy</subject><subject>Aurora Kinase B</subject><subject>Aurora Kinase C</subject><subject>Aurora Kinases</subject><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>Cellular Biology</subject><subject>Chromosome aberrations</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>genomic instability</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Male genital diseases</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>mitosis</subject><subject>Neoplasms, Germ Cell and Embryonal - genetics</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>RNA, Messenger</subject><subject>Seminoma - genetics</subject><subject>testicular germ cell tumour</subject><subject>Testicular Neoplasms - genetics</subject><subject>Testis - enzymology</subject><subject>Up-Regulation</subject><issn>0303-4569</issn><issn>1439-0272</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkVtr3DAQhUVpaZY0f6HopfSldnWxJBv6siRNUli2kPQCfRlke5xo48tWstPNv6_c3W4GhATzndFhDiGUs5TH-rhJeSaLhAkjUsFYkcaTm3T3giyOjZdkwSSTSaZ0cULOQtiwWJkyJstekxPBtCi0Ygtye4Ee76bWjm7o6dDQ5eQHb-mD621Aeoc9UtxtPYYwA66n91NnezpiGF0VdT4yvqMVti0dp26YfHhDXjW2DXh2uE_J98vP386vk9XXqy_ny1VSZUaapFRW1hx5zWopm7IpeF7nXCnToDZolOKlqjUqwSRmUhktS95o2RglS5PZSp6SD_u597aFrXed9U8wWAfXyxW4PkRfwJjiXAj9yCP-fo9v_fB7iv6hc2H2bXscpgBGyiLPmMkj-fZATmWH9XH2_7VF4N0BsKGybeNtX7nwzMn4LStU5D7tuT-uxadjnzOYk4QNzIHBHBjMScK_JGEHy_VFfER5spe7MOLuKLf-AXTcoIKf6yv4cfNL3ay1ACb_AjbDnrM</recordid><startdate>201008</startdate><enddate>201008</enddate><creator>Baldini, E.</creator><creator>Arlot-Bonnemains, Y.</creator><creator>Mottolese, M.</creator><creator>Sentinelli, S.</creator><creator>Antoniani, B.</creator><creator>Sorrenti, S.</creator><creator>Salducci, M.</creator><creator>Comini, E.</creator><creator>Ulisse, S.</creator><creator>D'Armiento, M.</creator><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</general><general>Wiley</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>1XC</scope></search><sort><creationdate>201008</creationdate><title>Deregulation of Aurora kinase gene expression in human testicular germ cell tumours</title><author>Baldini, E. ; Arlot-Bonnemains, Y. ; Mottolese, M. ; Sentinelli, S. ; Antoniani, B. ; Sorrenti, S. ; Salducci, M. ; Comini, E. ; Ulisse, S. ; D'Armiento, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4737-b5a3d1e1d0d33fbf918d81557fe67e7551b5d6e5203e435763b1f63f753b74ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Aneuploidy</topic><topic>Aurora Kinase B</topic><topic>Aurora Kinase C</topic><topic>Aurora Kinases</topic><topic>Biological and medical sciences</topic><topic>Cancer</topic><topic>Cellular Biology</topic><topic>Chromosome aberrations</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>genomic instability</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Male genital diseases</topic><topic>Medical genetics</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>mitosis</topic><topic>Neoplasms, Germ Cell and Embryonal - genetics</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>RNA, Messenger</topic><topic>Seminoma - genetics</topic><topic>testicular germ cell tumour</topic><topic>Testicular Neoplasms - genetics</topic><topic>Testis - enzymology</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Baldini, E.</creatorcontrib><creatorcontrib>Arlot-Bonnemains, Y.</creatorcontrib><creatorcontrib>Mottolese, M.</creatorcontrib><creatorcontrib>Sentinelli, S.</creatorcontrib><creatorcontrib>Antoniani, B.</creatorcontrib><creatorcontrib>Sorrenti, S.</creatorcontrib><creatorcontrib>Salducci, M.</creatorcontrib><creatorcontrib>Comini, E.</creatorcontrib><creatorcontrib>Ulisse, S.</creatorcontrib><creatorcontrib>D'Armiento, M.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Andrologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baldini, E.</au><au>Arlot-Bonnemains, Y.</au><au>Mottolese, M.</au><au>Sentinelli, S.</au><au>Antoniani, B.</au><au>Sorrenti, S.</au><au>Salducci, M.</au><au>Comini, E.</au><au>Ulisse, S.</au><au>D'Armiento, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deregulation of Aurora kinase gene expression in human testicular germ cell tumours</atitle><jtitle>Andrologia</jtitle><addtitle>Andrologia</addtitle><date>2010-08</date><risdate>2010</risdate><volume>42</volume><issue>4</issue><spage>260</spage><epage>267</epage><pages>260-267</pages><issn>0303-4569</issn><eissn>1439-0272</eissn><coden>ANDRDQ</coden><abstract><![CDATA[Summary The Aurora kinases regulate chromosome segregation and cytokinesis, and alterations in their expression associate with cell malignant transformation. In this study, we demonstrated by qRT‐PCR analysis of 14 seminomas that Aurora‐A mRNA was, with respect to control tissues, augmented in five of 14 tumour tissues by 2.17 ± 0.30 fold (P < 0.05) and reduced in 9 to 0.38 ± 0.10 (P < 0.01). Aurora‐B mRNA was increased in 11 tumour tissues by 4.33 ± 0.82 fold (P < 0.01) and reduced in 3 to 0.41 ± 0.11 fold. Aurora‐C mRNA was reduced to 0.20 ± 0.32 fold (P < 0.01) in 13 seminomas and up‐regulated in one case. Western blot experiments, performed on protein extracts of nine seminomas and six normal testes, showed an up‐regulation of Aurora‐B protein by 10.14 ± 3.51 fold (P < 0.05), while Aurora‐A protein was found increased in four seminomas by 2.16 ± 0.43 (P < 0.05), unchanged in three and reduced in two tumour tissues. Aurora‐C protein was increased by 9.2 ± 2.90 fold (P < 0.05), suggesting that post‐transcriptional mechanisms modulate its expression. In conclusion, we demonstrated that expression of Aurora kinases is deregulated in seminomas, suggesting that they may play a role in the progression of testicular cancers.]]></abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20629650</pmid><doi>10.1111/j.1439-0272.2009.00987.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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source Wiley Online Library - AutoHoldings Journals; MEDLINE
subjects Adult
Aneuploidy
Aurora Kinase B
Aurora Kinase C
Aurora Kinases
Biological and medical sciences
Cancer
Cellular Biology
Chromosome aberrations
Gene Expression Regulation, Neoplastic
genomic instability
Gynecology. Andrology. Obstetrics
Humans
Life Sciences
Male
Male genital diseases
Medical genetics
Medical sciences
Middle Aged
mitosis
Neoplasms, Germ Cell and Embryonal - genetics
Protein-Serine-Threonine Kinases - genetics
RNA, Messenger
Seminoma - genetics
testicular germ cell tumour
Testicular Neoplasms - genetics
Testis - enzymology
Up-Regulation
title Deregulation of Aurora kinase gene expression in human testicular germ cell tumours
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