The Gap Junctional Protein Connexin(Cx)43 in Testicular Cancer: its Loss Marks Progession from Carcinoma In Situ to Invasive Germ Cell Tumour
Identifieur interne : 001604 ( Istex/Corpus ); précédent : 001603; suivant : 001605The Gap Junctional Protein Connexin(Cx)43 in Testicular Cancer: its Loss Marks Progession from Carcinoma In Situ to Invasive Germ Cell Tumour
Auteurs : R. Brehm ; P. Fischer ; S. Kliesch ; I. Gashaw ; E. Winterhager ; R. M. Bohle ; K. Steger ; M. BergmannSource :
- Anatomia, Histologia, Embryologia [ 0340-2096 ] ; 2005-12.
Abstract
Carcinoma‐in‐situ (CIS) of the testis is known to be the pre‐invasive stage of most human germ cell tumours (seminoma and non‐seminoma), but the mechanisms leading to an increased pubertal proliferation of CIS cells after a long latency and to progression of CIS to an invasive malignancy are still not known. Additionally, CIS and seminoma have also been reported in equine testis (Veeramachaneni and Sawyer, 1998). The gap junctional protein and tumour suppressor gene connexin(cx)43 represents the predominant cx in human, canine and rodent testis so far and it is expected to play a key role for the regulation of both proliferation and differentiation of germ cells (spermatogonia and spermatocytes), and its gene‐ and protein‐expression pattern is typical for the pubertal terminal differentiation of somatic Sertoli cells. Using cDNA‐microarray analysis, in‐situ hybridization (ISH), RT‐PCR from tissue homogenate and semi‐quantitative RT‐PCR from well defined microdissected tubules with normal spermatogenesis, CIS, intratubular seminoma (ISe) and from seminoma cells from invasive seminoma we found a downregulation of cx43 starting in intratubular CIS, leading to a complete loss in most invasive seminoma cells. This indicates that regulation of cx43 expression takes place at transcriptional level confirming and expanding earlier studies of protein expression (Brehm et al., 2002). This reduction of cx43‐expression suggests that an early intratubular derangement in cx43‐gene expression and disruption of inter‐cellular communication between Sertoli cells and/or Sertoli cells and pre‐invasive tumour cells via cx43‐gap junctions may play a role in the proliferation of CIS cells and seminoma cells and in the progression phase of testicular seminoma development.
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DOI: 10.1111/j.1439-0264.2005.00669_16.x
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Bergmann</name><affiliation><mods:affiliation>Institute of Veterinary Anatomy, University of Giessen, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Anatomia, Histologia, Embryologia</title><idno type="ISSN">0340-2096</idno><idno type="eISSN">1439-0264</idno><imprint><publisher>Blackwell Verlag GmbH</publisher><pubPlace>Berlin, Germany</pubPlace><date type="published" when="2005-12">2005-12</date><biblScope unit="volume">34</biblScope><biblScope unit="supplement">s1</biblScope><biblScope unit="page" from="7">7</biblScope><biblScope unit="page" to="8">8</biblScope></imprint><idno type="ISSN">0340-2096</idno></series><idno type="istex">8B3C1F9A90C9B0F41181E5799A753F4CAFAD34CB</idno><idno type="DOI">10.1111/j.1439-0264.2005.00669_16.x</idno><idno type="ArticleID">AHE669_16_16</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0340-2096</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Carcinoma‐in‐situ (CIS) of the testis is known to be the pre‐invasive stage of most human germ cell tumours (seminoma and non‐seminoma), but the mechanisms leading to an increased pubertal proliferation of CIS cells after a long latency and to progression of CIS to an invasive malignancy are still not known. Additionally, CIS and seminoma have also been reported in equine testis (Veeramachaneni and Sawyer, 1998). The gap junctional protein and tumour suppressor gene connexin(cx)43 represents the predominant cx in human, canine and rodent testis so far and it is expected to play a key role for the regulation of both proliferation and differentiation of germ cells (spermatogonia and spermatocytes), and its gene‐ and protein‐expression pattern is typical for the pubertal terminal differentiation of somatic Sertoli cells. Using cDNA‐microarray analysis, in‐situ hybridization (ISH), RT‐PCR from tissue homogenate and semi‐quantitative RT‐PCR from well defined microdissected tubules with normal spermatogenesis, CIS, intratubular seminoma (ISe) and from seminoma cells from invasive seminoma we found a downregulation of cx43 starting in intratubular CIS, leading to a complete loss in most invasive seminoma cells. This indicates that regulation of cx43 expression takes place at transcriptional level confirming and expanding earlier studies of protein expression (Brehm et al., 2002). This reduction of cx43‐expression suggests that an early intratubular derangement in cx43‐gene expression and disruption of inter‐cellular communication between Sertoli cells and/or Sertoli cells and pre‐invasive tumour cells via cx43‐gap junctions may play a role in the proliferation of CIS cells and seminoma cells and in the progression phase of testicular seminoma development.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>R. Brehm</name><affiliations><json:string>Institute of Veterinary Anatomy, University of Giessen, Germany</json:string></affiliations></json:item><json:item><name>P. Fischer</name><affiliations><json:string>Institute of Veterinary Anatomy, University of Giessen, Germany</json:string></affiliations></json:item><json:item><name>S. 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M.</forename><surname>Bohle</surname></persName><affiliation>Department of Pathology, University of Giessen, Germany</affiliation></author><author xml:id="author-7"><persName><forename type="first">K.</forename><surname>Steger</surname></persName><affiliation>Institute of Veterinary Anatomy, University of Giessen, Germany</affiliation></author><author xml:id="author-8"><persName><forename type="first">M.</forename><surname>Bergmann</surname></persName><affiliation>Institute of Veterinary Anatomy, University of Giessen, Germany</affiliation></author></analytic><monogr><title level="j">Anatomia, Histologia, Embryologia</title><idno type="pISSN">0340-2096</idno><idno type="eISSN">1439-0264</idno><idno type="DOI">10.1111/(ISSN)1439-0264</idno><imprint><publisher>Blackwell Verlag GmbH</publisher><pubPlace>Berlin, Germany</pubPlace><date type="published" when="2005-12"></date><biblScope unit="volume">34</biblScope><biblScope unit="supplement">s1</biblScope><biblScope unit="page" from="7">7</biblScope><biblScope unit="page" to="8">8</biblScope></imprint></monogr><idno type="istex">8B3C1F9A90C9B0F41181E5799A753F4CAFAD34CB</idno><idno type="DOI">10.1111/j.1439-0264.2005.00669_16.x</idno><idno type="ArticleID">AHE669_16_16</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Carcinoma‐in‐situ (CIS) of the testis is known to be the pre‐invasive stage of most human germ cell tumours (seminoma and non‐seminoma), but the mechanisms leading to an increased pubertal proliferation of CIS cells after a long latency and to progression of CIS to an invasive malignancy are still not known. Additionally, CIS and seminoma have also been reported in equine testis (Veeramachaneni and Sawyer, 1998). The gap junctional protein and tumour suppressor gene connexin(cx)43 represents the predominant cx in human, canine and rodent testis so far and it is expected to play a key role for the regulation of both proliferation and differentiation of germ cells (spermatogonia and spermatocytes), and its gene‐ and protein‐expression pattern is typical for the pubertal terminal differentiation of somatic Sertoli cells. Using cDNA‐microarray analysis, in‐situ hybridization (ISH), RT‐PCR from tissue homogenate and semi‐quantitative RT‐PCR from well defined microdissected tubules with normal spermatogenesis, CIS, intratubular seminoma (ISe) and from seminoma cells from invasive seminoma we found a downregulation of cx43 starting in intratubular CIS, leading to a complete loss in most invasive seminoma cells. This indicates that regulation of cx43 expression takes place at transcriptional level confirming and expanding earlier studies of protein expression (Brehm et al., 2002). This reduction of cx43‐expression suggests that an early intratubular derangement in cx43‐gene expression and disruption of inter‐cellular communication between Sertoli cells and/or Sertoli cells and pre‐invasive tumour cells via cx43‐gap junctions may play a role in the proliferation of CIS cells and seminoma cells and in the progression phase of testicular seminoma development.</p></abstract><abstract><p>References Veeramachaneni, D. N., and H. R.Sawyer, 1998: Carcinoma in situ and seminoma in equine testis. APMIS 106, 183–185.</p></abstract><abstract><p>Brehm R., A. Marks, R. Rey, S. Kliesch, M. Bergmann and K. Steger, 2002: Altered expression of connexins 26 and 43 in Sertoli cells in seminiferous tubules infiltrated with carcinoma‐in‐situ or seminoma. J. Pathol. 197, 647–653.</p></abstract></profileDesc><revisionDesc><change when="2005-12">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-12-13">References added</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2017-02-8">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/8B3C1F9A90C9B0F41181E5799A753F4CAFAD34CB/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley component found"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Verlag GmbH</publisherName><publisherLoc>Berlin, Germany</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1439-0264</doi><issn type="print">0340-2096</issn><issn type="electronic">1439-0264</issn><idGroup><id type="product" value="AHE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ANATOMIA HISTOLOGIA EMBRYOLOGIA">Anatomia, Histologia, Embryologia</title></titleGroup></publicationMeta><publicationMeta level="part" position="12000"><doi origin="wiley">10.1111/ahe.2005.34.issue-s1</doi><numberingGroup><numbering type="journalVolume" number="34">34</numbering><numbering type="supplement">s1</numbering></numberingGroup><coverDate startDate="2005-12">December 2005</coverDate></publicationMeta><publicationMeta level="unit" type="abstract" position="1" status="forIssue"><doi origin="wiley">10.1111/j.1439-0264.2005.00669_16.x</doi><idGroup><id type="unit" value="AHE669_16_16"></id></idGroup><titleGroup><title type="tocHeading1">Abstracts of the XXVth Congress of the European Association of Veterinary Anatomists (EAVA), Oslo, 28–31 July 2004</title></titleGroup><eventGroup><event type="firstOnline" date="2005-11-22"></event><event type="publishedOnlineFinalForm" date="2005-11-22"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:Header result:Header" date="2010-04-14"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-01"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="7">7</numbering><numbering type="pageLast" number="8">8</numbering></numberingGroup><linkGroup><link type="toTypesetVersion" href="file:AHE.AHE669_16_16.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">The Gap Junctional Protein Connexin(Cx)43 in Testicular Cancer: its Loss Marks Progession from Carcinoma <i>In Situ</i> to Invasive Germ Cell Tumour</title><title type="short">Abstracts</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a16-1"><personName><givenNames>R.</givenNames><familyName>Brehm</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a16-1"><personName><givenNames>P.</givenNames><familyName>Fischer</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a16-2"><personName><givenNames>S.</givenNames><familyName>Kliesch</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a16-3"><personName><givenNames>I.</givenNames><familyName>Gashaw</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a16-3"><personName><givenNames>E.</givenNames><familyName>Winterhager</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a16-4"><personName><givenNames>R. M.</givenNames><familyName>Bohle</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a16-1"><personName><givenNames>K.</givenNames><familyName>Steger</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a16-1"><personName><givenNames>M.</givenNames><familyName>Bergmann</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a16-1" countryCode="DE"><unparsedAffiliation>Institute of Veterinary Anatomy, University of Giessen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a16-2" countryCode="DE"><unparsedAffiliation>Department of Urology, University of Muenster, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a16-3" countryCode="DE"><unparsedAffiliation>Institute of Anatomy, University Hospital, Essen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a16-4" countryCode="DE"><unparsedAffiliation>Department of Pathology, University of Giessen, Germany</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Carcinoma‐in‐situ (CIS) of the testis is known to be the pre‐invasive stage of most human germ cell tumours (seminoma and non‐seminoma), but the mechanisms leading to an increased pubertal proliferation of CIS cells after a long latency and to progression of CIS to an invasive malignancy are still not known. Additionally, CIS and seminoma have also been reported in equine testis (Veeramachaneni and Sawyer, 1998). The gap junctional protein and tumour suppressor gene connexin(cx)43 represents the predominant cx in human, canine and rodent testis so far and it is expected to play a key role for the regulation of both proliferation and differentiation of germ cells (spermatogonia and spermatocytes), and its gene‐ and protein‐expression pattern is typical for the pubertal terminal differentiation of somatic Sertoli cells. Using cDNA‐microarray analysis, in‐situ hybridization (ISH), RT‐PCR from tissue homogenate and semi‐quantitative RT‐PCR from well defined microdissected tubules with normal spermatogenesis, CIS, intratubular seminoma (ISe) and from seminoma cells from invasive seminoma we found a downregulation of cx43 starting in intratubular CIS, leading to a complete loss in most invasive seminoma cells. This indicates that regulation of cx43 expression takes place at transcriptional level confirming and expanding earlier studies of protein expression (Brehm et al., 2002). This reduction of cx43‐expression suggests that an early intratubular derangement in cx43‐gene expression and disruption of inter‐cellular communication between Sertoli cells and/or Sertoli cells and pre‐invasive tumour cells via cx43‐gap junctions may play a role in the proliferation of CIS cells and seminoma cells and in the progression phase of testicular seminoma development.</p><p><b>References </b> Veeramachaneni, D. N., and H. R.Sawyer, 1998: Carcinoma <i>in situ</i> and seminoma in equine testis. <i>APMIS</i> 106, 183–185.</p><p>Brehm R., A. Marks, R. Rey, S. Kliesch, M. Bergmann and K. Steger, 2002: Altered expression of connexins 26 and 43 in Sertoli cells in seminiferous tubules infiltrated with carcinoma‐in‐situ or seminoma. <i>J. Pathol</i>. 197, 647–653.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The Gap Junctional Protein Connexin(Cx)43 in Testicular Cancer: its Loss Marks Progession from Carcinoma In Situ to Invasive Germ Cell Tumour</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Abstracts</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The Gap Junctional Protein Connexin(Cx)43 in Testicular Cancer: its Loss Marks Progession from Carcinoma In Situ to Invasive Germ Cell Tumour</title></titleInfo><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Brehm</namePart><affiliation>Institute of Veterinary Anatomy, University of Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Fischer</namePart><affiliation>Institute of Veterinary Anatomy, University of Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Kliesch</namePart><affiliation>Department of Urology, University of Muenster, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Gashaw</namePart><affiliation>Institute of Anatomy, University Hospital, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Winterhager</namePart><affiliation>Institute of Anatomy, University Hospital, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. M.</namePart><namePart type="family">Bohle</namePart><affiliation>Department of Pathology, University of Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Steger</namePart><affiliation>Institute of Veterinary Anatomy, University of Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Bergmann</namePart><affiliation>Institute of Veterinary Anatomy, University of Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="abstract" displayLabel="abstract"></genre><originInfo><publisher>Blackwell Verlag GmbH</publisher><place><placeTerm type="text">Berlin, Germany</placeTerm></place><dateIssued encoding="w3cdtf">2005-12</dateIssued><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Carcinoma‐in‐situ (CIS) of the testis is known to be the pre‐invasive stage of most human germ cell tumours (seminoma and non‐seminoma), but the mechanisms leading to an increased pubertal proliferation of CIS cells after a long latency and to progression of CIS to an invasive malignancy are still not known. Additionally, CIS and seminoma have also been reported in equine testis (Veeramachaneni and Sawyer, 1998). The gap junctional protein and tumour suppressor gene connexin(cx)43 represents the predominant cx in human, canine and rodent testis so far and it is expected to play a key role for the regulation of both proliferation and differentiation of germ cells (spermatogonia and spermatocytes), and its gene‐ and protein‐expression pattern is typical for the pubertal terminal differentiation of somatic Sertoli cells. Using cDNA‐microarray analysis, in‐situ hybridization (ISH), RT‐PCR from tissue homogenate and semi‐quantitative RT‐PCR from well defined microdissected tubules with normal spermatogenesis, CIS, intratubular seminoma (ISe) and from seminoma cells from invasive seminoma we found a downregulation of cx43 starting in intratubular CIS, leading to a complete loss in most invasive seminoma cells. This indicates that regulation of cx43 expression takes place at transcriptional level confirming and expanding earlier studies of protein expression (Brehm et al., 2002). This reduction of cx43‐expression suggests that an early intratubular derangement in cx43‐gene expression and disruption of inter‐cellular communication between Sertoli cells and/or Sertoli cells and pre‐invasive tumour cells via cx43‐gap junctions may play a role in the proliferation of CIS cells and seminoma cells and in the progression phase of testicular seminoma development.</abstract><abstract>References Veeramachaneni, D. N., and H. R.Sawyer, 1998: Carcinoma in situ and seminoma in equine testis. APMIS 106, 183–185.</abstract><abstract>Brehm R., A. Marks, R. Rey, S. Kliesch, M. Bergmann and K. Steger, 2002: Altered expression of connexins 26 and 43 in Sertoli cells in seminiferous tubules infiltrated with carcinoma‐in‐situ or seminoma. J. Pathol. 197, 647–653.</abstract><relatedItem type="host"><titleInfo><title>Anatomia, Histologia, Embryologia</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0340-2096</identifier><identifier type="eISSN">1439-0264</identifier><identifier type="DOI">10.1111/(ISSN)1439-0264</identifier><identifier type="PublisherID">AHE</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>34</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>s1</number></detail><extent unit="pages"><start>7</start><end>8</end></extent></part></relatedItem><identifier type="istex">8B3C1F9A90C9B0F41181E5799A753F4CAFAD34CB</identifier><identifier type="DOI">10.1111/j.1439-0264.2005.00669_16.x</identifier><identifier type="ArticleID">AHE669_16_16</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Verlag GmbH</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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