Integrin clipping: A novel adhesion switch?
During human prostate cancer progression, the majority of normally expressed integrins are suppressed with the exception of the α6, α3, and β1 integrins. We have shown that in prostate cancer, the α6 integrin is found paired with the β1 integrin and that a novel form of the α6 integrin that lacks a...
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Veröffentlicht in: | Journal of cellular biochemistry 2004-01, Vol.91 (1), p.26-35 |
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description | During human prostate cancer progression, the majority of normally expressed integrins are suppressed with the exception of the α6, α3, and β1 integrins. We have shown that in prostate cancer, the α6 integrin is found paired with the β1 integrin and that a novel form of the α6 integrin that lacks a large portion of the extracellular domain (α6p) exists. The α6pβ1 integrin is found in human prostate cancer tissue specimens as well as tissue culture cell lines and is formed on the cell surface. This review discusses the mechanism of α6pβ1 production and the potential functions of this integrin variant. Our current working model predicts that the α6pβ1 integrin maintains the intracellular cytoskeletal connections associated with the heterodimer while allowing for an alteration in cell adhesion. The mechanism provides a selective advantage for cancer cell metastasis. © 2003 Wiley‐Liss, Inc. |
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We have shown that in prostate cancer, the α6 integrin is found paired with the β1 integrin and that a novel form of the α6 integrin that lacks a large portion of the extracellular domain (α6p) exists. The α6pβ1 integrin is found in human prostate cancer tissue specimens as well as tissue culture cell lines and is formed on the cell surface. This review discusses the mechanism of α6pβ1 production and the potential functions of this integrin variant. Our current working model predicts that the α6pβ1 integrin maintains the intracellular cytoskeletal connections associated with the heterodimer while allowing for an alteration in cell adhesion. The mechanism provides a selective advantage for cancer cell metastasis. © 2003 Wiley‐Liss, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.10675</identifier><identifier>PMID: 14689578</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>adhesion ; cancer progression ; Cell Adhesion ; Humans ; integrin ; Integrin alpha3 - metabolism ; Integrin alpha6 - metabolism ; Integrin beta1 - metabolism ; Male ; Prostatic Neoplasms - metabolism ; protease ; Protein Isoforms - metabolism ; Urokinase-Type Plasminogen Activator - metabolism</subject><ispartof>Journal of cellular biochemistry, 2004-01, Vol.91 (1), p.26-35</ispartof><rights>Copyright © 2003 Wiley‐Liss, Inc.</rights><rights>Copyright 2003 Wiley-Liss, Inc.</rights><rights>2003 Wiley-Liss, Inc. 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5155-d7e2968ae22dcfaffc90a7d4d7e318f01edb7583609747064a1c6b19f41fc9333</citedby><cites>FETCH-LOGICAL-c5155-d7e2968ae22dcfaffc90a7d4d7e318f01edb7583609747064a1c6b19f41fc9333</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.10675$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.10675$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14689578$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Demetriou, Manolis C.</creatorcontrib><creatorcontrib>Cress, Anne E.</creatorcontrib><title>Integrin clipping: A novel adhesion switch?</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>During human prostate cancer progression, the majority of normally expressed integrins are suppressed with the exception of the α6, α3, and β1 integrins. We have shown that in prostate cancer, the α6 integrin is found paired with the β1 integrin and that a novel form of the α6 integrin that lacks a large portion of the extracellular domain (α6p) exists. The α6pβ1 integrin is found in human prostate cancer tissue specimens as well as tissue culture cell lines and is formed on the cell surface. This review discusses the mechanism of α6pβ1 production and the potential functions of this integrin variant. Our current working model predicts that the α6pβ1 integrin maintains the intracellular cytoskeletal connections associated with the heterodimer while allowing for an alteration in cell adhesion. The mechanism provides a selective advantage for cancer cell metastasis. © 2003 Wiley‐Liss, Inc.</description><subject>adhesion</subject><subject>cancer progression</subject><subject>Cell Adhesion</subject><subject>Humans</subject><subject>integrin</subject><subject>Integrin alpha3 - metabolism</subject><subject>Integrin alpha6 - metabolism</subject><subject>Integrin beta1 - metabolism</subject><subject>Male</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>protease</subject><subject>Protein Isoforms - metabolism</subject><subject>Urokinase-Type Plasminogen Activator - metabolism</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kF1PwjAUhhujEUQv_ANmVybGTPq1dvNCA0QR40dCNF42peugOLa5DpB_b3WIeuFVT3qe85yTF4BDBM8QhLg9VSNXMB5sgSaCEfcpo3QbNCEn0McE4QbYs3YKIYwigndBA1EWRgEPm-B0kFV6XJrMU6kpCpONz72Ol-ULnXoynmhr8syzS1OpyeU-2ElkavXB-m2B5-urp96Nf_fYH_Q6d74KUBD4Mdc4YqHUGMcqkUmiIih5TN0_QWECkY5HPAgJc5dSDhmVSLERihKKHEoIaYGL2lvMRzMdK51VpUxFUZqZLFcil0b87WRmIsb5QmAOMSWhExyvBWX-Nte2EjNjlU5Tmel8bkUIIWMEBQ48qUFV5taWOtksQVB8RitctOIrWsce_b7qh1xn6YB2DSxNqlf_m8Rtr_ut9OsJYyv9vpmQ5atgnDjy5aEvhkPO70k3EEPyAdthkZs</recordid><startdate>20040101</startdate><enddate>20040101</enddate><creator>Demetriou, Manolis C.</creator><creator>Cress, Anne E.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040101</creationdate><title>Integrin clipping: A novel adhesion switch?</title><author>Demetriou, Manolis C. ; Cress, Anne E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5155-d7e2968ae22dcfaffc90a7d4d7e318f01edb7583609747064a1c6b19f41fc9333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>adhesion</topic><topic>cancer progression</topic><topic>Cell Adhesion</topic><topic>Humans</topic><topic>integrin</topic><topic>Integrin alpha3 - metabolism</topic><topic>Integrin alpha6 - metabolism</topic><topic>Integrin beta1 - metabolism</topic><topic>Male</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>protease</topic><topic>Protein Isoforms - metabolism</topic><topic>Urokinase-Type Plasminogen Activator - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Demetriou, Manolis C.</creatorcontrib><creatorcontrib>Cress, Anne E.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Demetriou, Manolis C.</au><au>Cress, Anne E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Integrin clipping: A novel adhesion switch?</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem</addtitle><date>2004-01-01</date><risdate>2004</risdate><volume>91</volume><issue>1</issue><spage>26</spage><epage>35</epage><pages>26-35</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>During human prostate cancer progression, the majority of normally expressed integrins are suppressed with the exception of the α6, α3, and β1 integrins. We have shown that in prostate cancer, the α6 integrin is found paired with the β1 integrin and that a novel form of the α6 integrin that lacks a large portion of the extracellular domain (α6p) exists. The α6pβ1 integrin is found in human prostate cancer tissue specimens as well as tissue culture cell lines and is formed on the cell surface. This review discusses the mechanism of α6pβ1 production and the potential functions of this integrin variant. 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subjects | adhesion cancer progression Cell Adhesion Humans integrin Integrin alpha3 - metabolism Integrin alpha6 - metabolism Integrin beta1 - metabolism Male Prostatic Neoplasms - metabolism protease Protein Isoforms - metabolism Urokinase-Type Plasminogen Activator - metabolism |
title | Integrin clipping: A novel adhesion switch? |
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