Expression and Functional Role of CCR9 in Prostate Cancer Cell Migration and Invasion
Purpose: Metastasis is responsible for most cancer-related deaths; hence, therapies designed to minimize metastasis are greatly needed. The precise cellular and molecular mechanisms used by cancer cells for metastasis are not fully understood; however, the metastatic spread of neoplastic cells is pr...
Gespeichert in:
| Veröffentlicht in: | Clinical cancer research 2004-12, Vol.10 (24), p.8743-8750 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 8750 |
|---|---|
| container_issue | 24 |
| container_start_page | 8743 |
| container_title | Clinical cancer research |
| container_volume | 10 |
| creator | SINGH, Shailesh SINGH, Udai P STILES, Jonathan K GRIZZLE, William E LILLARD, James W |
| description | Purpose: Metastasis is responsible for most cancer-related deaths; hence, therapies designed to minimize metastasis are greatly needed.
The precise cellular and molecular mechanisms used by cancer cells for metastasis are not fully understood; however, the metastatic
spread of neoplastic cells is probably related to the ability of these cells to migrate, invade, home, and survive locally.
The migration of tumor cells shares many similarities with leukocyte trafficking, which is regulated by chemokine receptor–ligand
interactions. The current study evaluates the molecular mechanisms of CCL25 and CCR9 in prostate cancer cell migration and
invasion.
Experimental Design: In the current study, real-time quantitative polymerase chain reaction, flow cytometry analysis, and in vitro migration as well as invasion chamber analysis (with and without antibody-mediated inhibition) were used to ascertain the
biological and functional significance of CCR9 expression by normal prostatic epithelial cells (PrEC) or prostate cancer cell
lines (LNCaP-10995 and PC3).
Results: We report that functional CCR9 is highly expressed by LNCaP cells and modestly, yet significantly, expressed by PC3 cells
when compared with PrEC cells. Neutralization of CCL25–CCR9 interactions impaired the migration and invasion potential of
the LNCaP and PC3 cell lines. CCL25 differentially modulated the expression of collagenase-1 or matrix metalloproteinase (MMP)-1,
collagenase-3 (MMP-13), stromalysin-2 (MMP-10), stromalysin-3 (MMP-11), and gelatinase-A (MMP-2), but not MMP-3, MMP-7, MMP-8,
MMP-9, MMP-12, or MMP-14 in prostate cancer cells.
Conclusions: These studies suggest that the expression and activation of CCR9 affect cancer cell migration, invasion, and MMP expression,
which together may affect prostate cancer metastasis. |
| doi_str_mv | 10.1158/1078-0432.CCR-04-0266 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67205574</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67205574</sourcerecordid><originalsourceid>FETCH-LOGICAL-c484t-5a42a3a7baee9e6e9b9fa7121baef8b70424e1730ca06a03b04620cd3e8e8eaa3</originalsourceid><addsrcrecordid>eNpFkElLxDAUgIMo7j9ByUXBQzVb0_YoZVxAUUTP4TXz6lQ67Zh0XP69r86I5JCX8L3tY-xIinMp0_xCiixPhNHqvCyfKEiEsnaD7co0zRKtbLpJ8R-zw_ZifBNCGinMNtuRqVXaWrHLXiZfi4AxNn3HoZvyq2XnB3pAy5_6Fnlfc6pf8Kbjj6GPAwzIS-g8Bl5i2_L75jXA8Jd9233AWOqAbdXQRjxc3_vs5WryXN4kdw_Xt-XlXeJNboYkBaNAQ1YBYoEWi6qoIZNK0kedV5kwyqDMtPAgLAhdCWOV8FONOR0Avc9OV3UXoX9fYhzcvIme5oIO-2V0NlOCfBgC0xXoaYkYsHaL0MwhfDsp3OjTja7c6MrRvhS40SflHa8bLKs5Tv-z1gIJOFkDED20dSA3TfznrC60lSlxZytu1rzOPpuAzv9aJPcIwc_GOZRxOc2qfwB2s4vC</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67205574</pqid></control><display><type>article</type><title>Expression and Functional Role of CCR9 in Prostate Cancer Cell Migration and Invasion</title><source>MEDLINE</source><source>American Association for Cancer Research Journals</source><source>Alma/SFX Local Collection</source><source>EZB Electronic Journals Library</source><creator>SINGH, Shailesh ; SINGH, Udai P ; STILES, Jonathan K ; GRIZZLE, William E ; LILLARD, James W</creator><creatorcontrib>SINGH, Shailesh ; SINGH, Udai P ; STILES, Jonathan K ; GRIZZLE, William E ; LILLARD, James W</creatorcontrib><description>Purpose: Metastasis is responsible for most cancer-related deaths; hence, therapies designed to minimize metastasis are greatly needed.
The precise cellular and molecular mechanisms used by cancer cells for metastasis are not fully understood; however, the metastatic
spread of neoplastic cells is probably related to the ability of these cells to migrate, invade, home, and survive locally.
The migration of tumor cells shares many similarities with leukocyte trafficking, which is regulated by chemokine receptor–ligand
interactions. The current study evaluates the molecular mechanisms of CCL25 and CCR9 in prostate cancer cell migration and
invasion.
Experimental Design: In the current study, real-time quantitative polymerase chain reaction, flow cytometry analysis, and in vitro migration as well as invasion chamber analysis (with and without antibody-mediated inhibition) were used to ascertain the
biological and functional significance of CCR9 expression by normal prostatic epithelial cells (PrEC) or prostate cancer cell
lines (LNCaP-10995 and PC3).
Results: We report that functional CCR9 is highly expressed by LNCaP cells and modestly, yet significantly, expressed by PC3 cells
when compared with PrEC cells. Neutralization of CCL25–CCR9 interactions impaired the migration and invasion potential of
the LNCaP and PC3 cell lines. CCL25 differentially modulated the expression of collagenase-1 or matrix metalloproteinase (MMP)-1,
collagenase-3 (MMP-13), stromalysin-2 (MMP-10), stromalysin-3 (MMP-11), and gelatinase-A (MMP-2), but not MMP-3, MMP-7, MMP-8,
MMP-9, MMP-12, or MMP-14 in prostate cancer cells.
Conclusions: These studies suggest that the expression and activation of CCR9 affect cancer cell migration, invasion, and MMP expression,
which together may affect prostate cancer metastasis.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-04-0266</identifier><identifier>PMID: 15623660</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adenocarcinoma - metabolism ; Adenocarcinoma - secondary ; Antineoplastic agents ; Biological and medical sciences ; Cell Movement ; Chemokines, CC - genetics ; Chemokines, CC - metabolism ; Epithelial Cells - metabolism ; Flow Cytometry ; Gene Expression Regulation, Neoplastic ; Gynecology. Andrology. Obstetrics ; Humans ; Male ; Male genital diseases ; Matrix Metalloproteinases - genetics ; Matrix Metalloproteinases - metabolism ; Medical sciences ; Neoplasm Invasiveness - pathology ; Nephrology. Urinary tract diseases ; Pharmacology. Drug treatments ; Prostate - metabolism ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Receptors, CCR ; Receptors, Chemokine - genetics ; Receptors, Chemokine - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; Tumor Cells, Cultured ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>Clinical cancer research, 2004-12, Vol.10 (24), p.8743-8750</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c484t-5a42a3a7baee9e6e9b9fa7121baef8b70424e1730ca06a03b04620cd3e8e8eaa3</citedby><cites>FETCH-LOGICAL-c484t-5a42a3a7baee9e6e9b9fa7121baef8b70424e1730ca06a03b04620cd3e8e8eaa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3342,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16393615$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15623660$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SINGH, Shailesh</creatorcontrib><creatorcontrib>SINGH, Udai P</creatorcontrib><creatorcontrib>STILES, Jonathan K</creatorcontrib><creatorcontrib>GRIZZLE, William E</creatorcontrib><creatorcontrib>LILLARD, James W</creatorcontrib><title>Expression and Functional Role of CCR9 in Prostate Cancer Cell Migration and Invasion</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: Metastasis is responsible for most cancer-related deaths; hence, therapies designed to minimize metastasis are greatly needed.
The precise cellular and molecular mechanisms used by cancer cells for metastasis are not fully understood; however, the metastatic
spread of neoplastic cells is probably related to the ability of these cells to migrate, invade, home, and survive locally.
The migration of tumor cells shares many similarities with leukocyte trafficking, which is regulated by chemokine receptor–ligand
interactions. The current study evaluates the molecular mechanisms of CCL25 and CCR9 in prostate cancer cell migration and
invasion.
Experimental Design: In the current study, real-time quantitative polymerase chain reaction, flow cytometry analysis, and in vitro migration as well as invasion chamber analysis (with and without antibody-mediated inhibition) were used to ascertain the
biological and functional significance of CCR9 expression by normal prostatic epithelial cells (PrEC) or prostate cancer cell
lines (LNCaP-10995 and PC3).
Results: We report that functional CCR9 is highly expressed by LNCaP cells and modestly, yet significantly, expressed by PC3 cells
when compared with PrEC cells. Neutralization of CCL25–CCR9 interactions impaired the migration and invasion potential of
the LNCaP and PC3 cell lines. CCL25 differentially modulated the expression of collagenase-1 or matrix metalloproteinase (MMP)-1,
collagenase-3 (MMP-13), stromalysin-2 (MMP-10), stromalysin-3 (MMP-11), and gelatinase-A (MMP-2), but not MMP-3, MMP-7, MMP-8,
MMP-9, MMP-12, or MMP-14 in prostate cancer cells.
Conclusions: These studies suggest that the expression and activation of CCR9 affect cancer cell migration, invasion, and MMP expression,
which together may affect prostate cancer metastasis.</description><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - secondary</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Cell Movement</subject><subject>Chemokines, CC - genetics</subject><subject>Chemokines, CC - metabolism</subject><subject>Epithelial Cells - metabolism</subject><subject>Flow Cytometry</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Male</subject><subject>Male genital diseases</subject><subject>Matrix Metalloproteinases - genetics</subject><subject>Matrix Metalloproteinases - metabolism</subject><subject>Medical sciences</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Pharmacology. Drug treatments</subject><subject>Prostate - metabolism</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Receptors, CCR</subject><subject>Receptors, Chemokine - genetics</subject><subject>Receptors, Chemokine - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkElLxDAUgIMo7j9ByUXBQzVb0_YoZVxAUUTP4TXz6lQ67Zh0XP69r86I5JCX8L3tY-xIinMp0_xCiixPhNHqvCyfKEiEsnaD7co0zRKtbLpJ8R-zw_ZifBNCGinMNtuRqVXaWrHLXiZfi4AxNn3HoZvyq2XnB3pAy5_6Fnlfc6pf8Kbjj6GPAwzIS-g8Bl5i2_L75jXA8Jd9233AWOqAbdXQRjxc3_vs5WryXN4kdw_Xt-XlXeJNboYkBaNAQ1YBYoEWi6qoIZNK0kedV5kwyqDMtPAgLAhdCWOV8FONOR0Avc9OV3UXoX9fYhzcvIme5oIO-2V0NlOCfBgC0xXoaYkYsHaL0MwhfDsp3OjTja7c6MrRvhS40SflHa8bLKs5Tv-z1gIJOFkDED20dSA3TfznrC60lSlxZytu1rzOPpuAzv9aJPcIwc_GOZRxOc2qfwB2s4vC</recordid><startdate>20041215</startdate><enddate>20041215</enddate><creator>SINGH, Shailesh</creator><creator>SINGH, Udai P</creator><creator>STILES, Jonathan K</creator><creator>GRIZZLE, William E</creator><creator>LILLARD, James W</creator><general>American Association for Cancer Research</general><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></search><sort><creationdate>20041215</creationdate><title>Expression and Functional Role of CCR9 in Prostate Cancer Cell Migration and Invasion</title><author>SINGH, Shailesh ; SINGH, Udai P ; STILES, Jonathan K ; GRIZZLE, William E ; LILLARD, James W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c484t-5a42a3a7baee9e6e9b9fa7121baef8b70424e1730ca06a03b04620cd3e8e8eaa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - secondary</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Cell Movement</topic><topic>Chemokines, CC - genetics</topic><topic>Chemokines, CC - metabolism</topic><topic>Epithelial Cells - metabolism</topic><topic>Flow Cytometry</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Male</topic><topic>Male genital diseases</topic><topic>Matrix Metalloproteinases - genetics</topic><topic>Matrix Metalloproteinases - metabolism</topic><topic>Medical sciences</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Pharmacology. Drug treatments</topic><topic>Prostate - metabolism</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Receptors, CCR</topic><topic>Receptors, Chemokine - genetics</topic><topic>Receptors, Chemokine - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SINGH, Shailesh</creatorcontrib><creatorcontrib>SINGH, Udai P</creatorcontrib><creatorcontrib>STILES, Jonathan K</creatorcontrib><creatorcontrib>GRIZZLE, William E</creatorcontrib><creatorcontrib>LILLARD, James W</creatorcontrib><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><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SINGH, Shailesh</au><au>SINGH, Udai P</au><au>STILES, Jonathan K</au><au>GRIZZLE, William E</au><au>LILLARD, James W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression and Functional Role of CCR9 in Prostate Cancer Cell Migration and Invasion</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2004-12-15</date><risdate>2004</risdate><volume>10</volume><issue>24</issue><spage>8743</spage><epage>8750</epage><pages>8743-8750</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Purpose: Metastasis is responsible for most cancer-related deaths; hence, therapies designed to minimize metastasis are greatly needed.
The precise cellular and molecular mechanisms used by cancer cells for metastasis are not fully understood; however, the metastatic
spread of neoplastic cells is probably related to the ability of these cells to migrate, invade, home, and survive locally.
The migration of tumor cells shares many similarities with leukocyte trafficking, which is regulated by chemokine receptor–ligand
interactions. The current study evaluates the molecular mechanisms of CCL25 and CCR9 in prostate cancer cell migration and
invasion.
Experimental Design: In the current study, real-time quantitative polymerase chain reaction, flow cytometry analysis, and in vitro migration as well as invasion chamber analysis (with and without antibody-mediated inhibition) were used to ascertain the
biological and functional significance of CCR9 expression by normal prostatic epithelial cells (PrEC) or prostate cancer cell
lines (LNCaP-10995 and PC3).
Results: We report that functional CCR9 is highly expressed by LNCaP cells and modestly, yet significantly, expressed by PC3 cells
when compared with PrEC cells. Neutralization of CCL25–CCR9 interactions impaired the migration and invasion potential of
the LNCaP and PC3 cell lines. CCL25 differentially modulated the expression of collagenase-1 or matrix metalloproteinase (MMP)-1,
collagenase-3 (MMP-13), stromalysin-2 (MMP-10), stromalysin-3 (MMP-11), and gelatinase-A (MMP-2), but not MMP-3, MMP-7, MMP-8,
MMP-9, MMP-12, or MMP-14 in prostate cancer cells.
Conclusions: These studies suggest that the expression and activation of CCR9 affect cancer cell migration, invasion, and MMP expression,
which together may affect prostate cancer metastasis.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>15623660</pmid><doi>10.1158/1078-0432.CCR-04-0266</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1078-0432 |
| ispartof | Clinical cancer research, 2004-12, Vol.10 (24), p.8743-8750 |
| issn | 1078-0432 1557-3265 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67205574 |
| source | MEDLINE; American Association for Cancer Research Journals; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Adenocarcinoma - metabolism Adenocarcinoma - secondary Antineoplastic agents Biological and medical sciences Cell Movement Chemokines, CC - genetics Chemokines, CC - metabolism Epithelial Cells - metabolism Flow Cytometry Gene Expression Regulation, Neoplastic Gynecology. Andrology. Obstetrics Humans Male Male genital diseases Matrix Metalloproteinases - genetics Matrix Metalloproteinases - metabolism Medical sciences Neoplasm Invasiveness - pathology Nephrology. Urinary tract diseases Pharmacology. Drug treatments Prostate - metabolism Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Receptors, CCR Receptors, Chemokine - genetics Receptors, Chemokine - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis Tumor Cells, Cultured Tumors Tumors of the urinary system Urinary tract. Prostate gland |
| title | Expression and Functional Role of CCR9 in Prostate Cancer Cell Migration and Invasion |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T20%3A12%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Expression%20and%20Functional%20Role%20of%20CCR9%20in%20Prostate%20Cancer%20Cell%20Migration%20and%20Invasion&rft.jtitle=Clinical%20cancer%20research&rft.au=SINGH,%20Shailesh&rft.date=2004-12-15&rft.volume=10&rft.issue=24&rft.spage=8743&rft.epage=8750&rft.pages=8743-8750&rft.issn=1078-0432&rft.eissn=1557-3265&rft_id=info:doi/10.1158/1078-0432.CCR-04-0266&rft_dat=%3Cproquest_cross%3E67205574%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=67205574&rft_id=info:pmid/15623660&rfr_iscdi=true |