Prostate cancer progression into androgen independency is associated with alterations in cell adhesion and invasivity

Background Mortality in prostate cancer is primarily due to failure to cure hormone refractory patients with metastatic disease. The present study focused on elucidating alterations in invasive properties, which are connected with progression into androgen independency. Methods Ability to grow witho...

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Veröffentlicht in:Prostate 2006-11, Vol.66 (15), p.1631-1640
Hauptverfasser: Jennbacken, Karin, Gustavsson, Heléne, Welén, Karin, Vallbo, Christina, Damber, Jan-Erik
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container_end_page 1640
container_issue 15
container_start_page 1631
container_title Prostate
container_volume 66
creator Jennbacken, Karin
Gustavsson, Heléne
Welén, Karin
Vallbo, Christina
Damber, Jan-Erik
description Background Mortality in prostate cancer is primarily due to failure to cure hormone refractory patients with metastatic disease. The present study focused on elucidating alterations in invasive properties, which are connected with progression into androgen independency. Methods Ability to grow without anchor, migration, cell adhesion properties and expression of invasive factors were investigated in LNCaP and its androgen‐independent subline LNCaP‐19. Also, invasive capacity into blood vessels was examined in subcutaneous tumors. Results Transition into an androgen‐independent state was associated with ability to grow without anchor, increased migration, and alterations in cell adhesion properties. The tumor suppressor E‐cadherin was downregulated and the proinvasive factors N‐cadherin, MMP‐9, and membrane type 1 (MT1)‐MMP were upregulated in LNCaP‐19. In addition, LNCaP‐19 displayed a markedly increased invasivity into blood vessels. Conclusions The results show that LNCaP‐19 mimics hormone refractory prostate cancer and therefore is an excellent tool for studies on androgen‐independent cancer and invasion. This study shows that transition into an androgen‐independent state correlates with several proinvasive alterations. Prostate 66: 1631–1640, 2006. © 2006 Wiley‐Liss, Inc.
doi_str_mv 10.1002/pros.20469
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The present study focused on elucidating alterations in invasive properties, which are connected with progression into androgen independency. Methods Ability to grow without anchor, migration, cell adhesion properties and expression of invasive factors were investigated in LNCaP and its androgen‐independent subline LNCaP‐19. Also, invasive capacity into blood vessels was examined in subcutaneous tumors. Results Transition into an androgen‐independent state was associated with ability to grow without anchor, increased migration, and alterations in cell adhesion properties. The tumor suppressor E‐cadherin was downregulated and the proinvasive factors N‐cadherin, MMP‐9, and membrane type 1 (MT1)‐MMP were upregulated in LNCaP‐19. In addition, LNCaP‐19 displayed a markedly increased invasivity into blood vessels. Conclusions The results show that LNCaP‐19 mimics hormone refractory prostate cancer and therefore is an excellent tool for studies on androgen‐independent cancer and invasion. This study shows that transition into an androgen‐independent state correlates with several proinvasive alterations. Prostate 66: 1631–1640, 2006. © 2006 Wiley‐Liss, Inc.</description><identifier>ISSN: 0270-4137</identifier><identifier>EISSN: 1097-0045</identifier><identifier>DOI: 10.1002/pros.20469</identifier><identifier>PMID: 16927303</identifier><identifier>CODEN: PRSTDS</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adenocarcinoma - genetics ; Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; androgen independent ; Androgens - metabolism ; Animals ; Biological and medical sciences ; cadherin ; Cell Adhesion - physiology ; Cell Adhesion Molecules - genetics ; Cell Adhesion Molecules - metabolism ; Cell Line, Tumor ; Cell Transformation, Neoplastic - metabolism ; Cell Transformation, Neoplastic - pathology ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Gynecology. Andrology. Obstetrics ; hormone refractory ; Humans ; integrin ; LNCaP ; LNCaP • androgen independent • hormone refractory • cadherin • integrin • MMP ; Male ; Male genital diseases ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MMP ; Neoplasm Invasiveness - pathology ; Neoplasm Invasiveness - physiopathology ; Nephrology. Urinary tract diseases ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Tumors ; Tumors of the urinary system ; Urinary tract. 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The present study focused on elucidating alterations in invasive properties, which are connected with progression into androgen independency. Methods Ability to grow without anchor, migration, cell adhesion properties and expression of invasive factors were investigated in LNCaP and its androgen‐independent subline LNCaP‐19. Also, invasive capacity into blood vessels was examined in subcutaneous tumors. Results Transition into an androgen‐independent state was associated with ability to grow without anchor, increased migration, and alterations in cell adhesion properties. The tumor suppressor E‐cadherin was downregulated and the proinvasive factors N‐cadherin, MMP‐9, and membrane type 1 (MT1)‐MMP were upregulated in LNCaP‐19. In addition, LNCaP‐19 displayed a markedly increased invasivity into blood vessels. Conclusions The results show that LNCaP‐19 mimics hormone refractory prostate cancer and therefore is an excellent tool for studies on androgen‐independent cancer and invasion. This study shows that transition into an androgen‐independent state correlates with several proinvasive alterations. Prostate 66: 1631–1640, 2006. © 2006 Wiley‐Liss, Inc.</description><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>androgen independent</subject><subject>Androgens - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>cadherin</subject><subject>Cell Adhesion - physiology</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cell Transformation, Neoplastic - pathology</subject><subject>Disease Progression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>hormone refractory</subject><subject>Humans</subject><subject>integrin</subject><subject>LNCaP</subject><subject>LNCaP • androgen independent • hormone refractory • cadherin • integrin • MMP</subject><subject>Male</subject><subject>Male genital diseases</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MMP</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Neoplasm Invasiveness - physiopathology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><subject>Urologi och njurmedicin</subject><subject>Urology and Nephrology</subject><issn>0270-4137</issn><issn>1097-0045</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU9v1DAQxS0EokvhwgdAvsABkeJ_iZNjVWBBqugKCki9WF57sjVkk5BJuuy3Z7a7tDcky5ZHv_dGM4-x51KcSCHU237o8EQJU1QP2EyKymZCmPwhmwllRWaktkfsCeJPIQgX6jE7kkWlrBZ6xqYFiUc_Ag--DTBwMlsNgJi6lqd27LhvI5Vg94vQA11t2PKE3CN2IZE08k0ar7lvRhj8SEIklgdoGu7jNdxakQsVbzymmzRun7JHtW8Qnh3eY_btw_vLs4_Z-cX809npeRaMVlUWgjGlVSHGOijlcx8DQB6DyXMDS6lyFaEUtVXWLlWMMq9ssErEqrSFrqXVx-zN3hc30E9L1w9p7Yet63xyq6l3VFpNDsEZTQrCX-1xWsLvCXB064S7OXwL3YSuKMuKTkHg6z0YaHs4QH3nLIXbZeJ2mbjbTAh-cXCdlmuI9-ghBAJeHgCPwTf1QEkkvOdKRfMqQ5zcc5vUwPY_Ld3iy8XXf82zvSbhCH_uNH745Qqrbe5-fJ67Szm_-q7fLdyV_gtmzbcf</recordid><startdate>200611</startdate><enddate>200611</enddate><creator>Jennbacken, Karin</creator><creator>Gustavsson, Heléne</creator><creator>Welén, Karin</creator><creator>Vallbo, Christina</creator><creator>Damber, Jan-Erik</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</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>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>F1U</scope></search><sort><creationdate>200611</creationdate><title>Prostate cancer progression into androgen independency is associated with alterations in cell adhesion and invasivity</title><author>Jennbacken, Karin ; Gustavsson, Heléne ; Welén, Karin ; Vallbo, Christina ; Damber, Jan-Erik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4329-cc44872cddfc22a5adcee5dc4554eb1252de80f7277b2dd1597c720d98763f173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>androgen independent</topic><topic>Androgens - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>cadherin</topic><topic>Cell Adhesion - physiology</topic><topic>Cell Adhesion Molecules - genetics</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cell Transformation, Neoplastic - pathology</topic><topic>Disease Progression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>hormone refractory</topic><topic>Humans</topic><topic>integrin</topic><topic>LNCaP</topic><topic>LNCaP • androgen independent • hormone refractory • cadherin • integrin • MMP</topic><topic>Male</topic><topic>Male genital diseases</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MMP</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Neoplasm Invasiveness - physiopathology</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><topic>Urologi och njurmedicin</topic><topic>Urology and Nephrology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jennbacken, Karin</creatorcontrib><creatorcontrib>Gustavsson, Heléne</creatorcontrib><creatorcontrib>Welén, Karin</creatorcontrib><creatorcontrib>Vallbo, Christina</creatorcontrib><creatorcontrib>Damber, Jan-Erik</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>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>Prostate</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jennbacken, Karin</au><au>Gustavsson, Heléne</au><au>Welén, Karin</au><au>Vallbo, Christina</au><au>Damber, Jan-Erik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prostate cancer progression into androgen independency is associated with alterations in cell adhesion and invasivity</atitle><jtitle>Prostate</jtitle><addtitle>Prostate</addtitle><date>2006-11</date><risdate>2006</risdate><volume>66</volume><issue>15</issue><spage>1631</spage><epage>1640</epage><pages>1631-1640</pages><issn>0270-4137</issn><eissn>1097-0045</eissn><coden>PRSTDS</coden><abstract>Background Mortality in prostate cancer is primarily due to failure to cure hormone refractory patients with metastatic disease. The present study focused on elucidating alterations in invasive properties, which are connected with progression into androgen independency. Methods Ability to grow without anchor, migration, cell adhesion properties and expression of invasive factors were investigated in LNCaP and its androgen‐independent subline LNCaP‐19. Also, invasive capacity into blood vessels was examined in subcutaneous tumors. Results Transition into an androgen‐independent state was associated with ability to grow without anchor, increased migration, and alterations in cell adhesion properties. The tumor suppressor E‐cadherin was downregulated and the proinvasive factors N‐cadherin, MMP‐9, and membrane type 1 (MT1)‐MMP were upregulated in LNCaP‐19. In addition, LNCaP‐19 displayed a markedly increased invasivity into blood vessels. Conclusions The results show that LNCaP‐19 mimics hormone refractory prostate cancer and therefore is an excellent tool for studies on androgen‐independent cancer and invasion. This study shows that transition into an androgen‐independent state correlates with several proinvasive alterations. Prostate 66: 1631–1640, 2006. © 2006 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>16927303</pmid><doi>10.1002/pros.20469</doi><tpages>10</tpages></addata></record>
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subjects Adenocarcinoma - genetics
Adenocarcinoma - metabolism
Adenocarcinoma - pathology
androgen independent
Androgens - metabolism
Animals
Biological and medical sciences
cadherin
Cell Adhesion - physiology
Cell Adhesion Molecules - genetics
Cell Adhesion Molecules - metabolism
Cell Line, Tumor
Cell Transformation, Neoplastic - metabolism
Cell Transformation, Neoplastic - pathology
Disease Progression
Gene Expression Regulation, Neoplastic
Gynecology. Andrology. Obstetrics
hormone refractory
Humans
integrin
LNCaP
LNCaP • androgen independent • hormone refractory • cadherin • integrin • MMP
Male
Male genital diseases
Medical sciences
Mice
Mice, Inbred BALB C
Mice, Nude
MMP
Neoplasm Invasiveness - pathology
Neoplasm Invasiveness - physiopathology
Nephrology. Urinary tract diseases
Prostatic Neoplasms - genetics
Prostatic Neoplasms - metabolism
Prostatic Neoplasms - pathology
Tumors
Tumors of the urinary system
Urinary tract. Prostate gland
Urologi och njurmedicin
Urology and Nephrology
title Prostate cancer progression into androgen independency is associated with alterations in cell adhesion and invasivity
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