Human laminin-5 and laminin-10 mediated gene expression of prostate carcinoma cells
In prostate cancer progression, the basal lamina switches from predominantly laminin‐5 to laminin‐10. DU‐145 prostate cancer cells were treated with either soluble laminin‐5 (20 ng/ml) or laminin‐10 (1 µg/ml) for 6, 24, and 48 hr. Total RNA was harvested for a 7,500 human cDNA microarray. Hybridizat...
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| Veröffentlicht in: | The Prostate 2006-09, Vol.66 (13), p.1381-1390 |
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| container_title | The Prostate |
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| creator | Calaluce, Robert Beck, Shaleen K. Bair, Elisabeth L. Pandey, Ritu Greer, Kevin A. Hoying, Adam M. Hoying, James B. Mount, David W. Nagle, Raymond B. |
| description | In prostate cancer progression, the basal lamina switches from predominantly laminin‐5 to laminin‐10. DU‐145 prostate cancer cells were treated with either soluble laminin‐5 (20 ng/ml) or laminin‐10 (1 µg/ml) for 6, 24, and 48 hr. Total RNA was harvested for a 7,500 human cDNA microarray. Hybridizations were carried out in accordance with a 10 sample analysis of variance (ANOVA) statistical model. One thousand one hundred sixteen genes had measurable expression 2 standard deviations above background and 50% of spots for any given sample for all hybridizations were positive. Expression values of significantly varying genes were clustered and a list of 408 genes (P |
| doi_str_mv | 10.1002/pros.20393 |
| format | Article |
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DU‐145 prostate cancer cells were treated with either soluble laminin‐5 (20 ng/ml) or laminin‐10 (1 µg/ml) for 6, 24, and 48 hr. Total RNA was harvested for a 7,500 human cDNA microarray. Hybridizations were carried out in accordance with a 10 sample analysis of variance (ANOVA) statistical model. One thousand one hundred sixteen genes had measurable expression 2 standard deviations above background and 50% of spots for any given sample for all hybridizations were positive. Expression values of significantly varying genes were clustered and a list of 408 genes (P < 0.05) with a 1.5 or greater fold change in at least one time point were chosen for further analysis. Seventy eight changed in a time‐dependent manner with laminin‐10 treatment, 85 changed with laminin‐5, and 13 showed changes with both treatments. The 408 genes that passed a paired t‐test in at least one time‐dependent category were further analyzed using Pathway Miner. One of the largest gene association networks involved signal transduction in the growth factor‐MAP kinase pathways. EGFR was validated by real‐time PCR and laminin‐10 mediated cell adhesion activated EGFR in DU‐145 cells. Both laminins appear to be important signal transducers in prostate cancer. Prostate 66: 1381–1390, 2006. © 2006 Wiley‐Liss, Inc.</description><identifier>ISSN: 0270-4137</identifier><identifier>EISSN: 1097-0045</identifier><identifier>DOI: 10.1002/pros.20393</identifier><identifier>PMID: 16804886</identifier><identifier>CODEN: PRSTDS</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Biological and medical sciences ; Calpain - genetics ; Calpain - metabolism ; cDNA microarray ; Cell Adhesion Molecules - physiology ; Cell Line, Tumor ; DNA, Neoplasm - genetics ; ErbB Receptors - genetics ; ErbB Receptors - metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Expression Regulation, Neoplastic - genetics ; Gynecology. Andrology. Obstetrics ; Humans ; Kalinin ; Laminin - physiology ; laminin-10 ; laminin-5 ; Male ; Male genital diseases ; MAP Kinase Signaling System - genetics ; Medical sciences ; Nephrology. Urinary tract diseases ; Oligonucleotide Array Sequence Analysis ; prostate carcinoma cells ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; RNA, Neoplasm - genetics ; signal transduction ; Signal Transduction - genetics ; Time Factors ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>The Prostate, 2006-09, Vol.66 (13), p.1381-1390</ispartof><rights>Copyright © 2006 Wiley‐Liss, Inc., A Wiley Company</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3953-e7029974cfdcc47618d582f89ad9bfa4bc618a53ebc0bc1b10272bec039310a63</citedby><cites>FETCH-LOGICAL-c3953-e7029974cfdcc47618d582f89ad9bfa4bc618a53ebc0bc1b10272bec039310a63</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%2Fpros.20393$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpros.20393$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18120410$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16804886$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Calaluce, Robert</creatorcontrib><creatorcontrib>Beck, Shaleen K.</creatorcontrib><creatorcontrib>Bair, Elisabeth L.</creatorcontrib><creatorcontrib>Pandey, Ritu</creatorcontrib><creatorcontrib>Greer, Kevin A.</creatorcontrib><creatorcontrib>Hoying, Adam M.</creatorcontrib><creatorcontrib>Hoying, James B.</creatorcontrib><creatorcontrib>Mount, David W.</creatorcontrib><creatorcontrib>Nagle, Raymond B.</creatorcontrib><title>Human laminin-5 and laminin-10 mediated gene expression of prostate carcinoma cells</title><title>The Prostate</title><addtitle>Prostate</addtitle><description>In prostate cancer progression, the basal lamina switches from predominantly laminin‐5 to laminin‐10. DU‐145 prostate cancer cells were treated with either soluble laminin‐5 (20 ng/ml) or laminin‐10 (1 µg/ml) for 6, 24, and 48 hr. Total RNA was harvested for a 7,500 human cDNA microarray. Hybridizations were carried out in accordance with a 10 sample analysis of variance (ANOVA) statistical model. One thousand one hundred sixteen genes had measurable expression 2 standard deviations above background and 50% of spots for any given sample for all hybridizations were positive. Expression values of significantly varying genes were clustered and a list of 408 genes (P < 0.05) with a 1.5 or greater fold change in at least one time point were chosen for further analysis. Seventy eight changed in a time‐dependent manner with laminin‐10 treatment, 85 changed with laminin‐5, and 13 showed changes with both treatments. The 408 genes that passed a paired t‐test in at least one time‐dependent category were further analyzed using Pathway Miner. One of the largest gene association networks involved signal transduction in the growth factor‐MAP kinase pathways. EGFR was validated by real‐time PCR and laminin‐10 mediated cell adhesion activated EGFR in DU‐145 cells. Both laminins appear to be important signal transducers in prostate cancer. Prostate 66: 1381–1390, 2006. © 2006 Wiley‐Liss, Inc.</description><subject>Biological and medical sciences</subject><subject>Calpain - genetics</subject><subject>Calpain - metabolism</subject><subject>cDNA microarray</subject><subject>Cell Adhesion Molecules - physiology</subject><subject>Cell Line, Tumor</subject><subject>DNA, Neoplasm - genetics</subject><subject>ErbB Receptors - genetics</subject><subject>ErbB Receptors - metabolism</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Kalinin</subject><subject>Laminin - physiology</subject><subject>laminin-10</subject><subject>laminin-5</subject><subject>Male</subject><subject>Male genital diseases</subject><subject>MAP Kinase Signaling System - genetics</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>prostate carcinoma cells</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>RNA, Neoplasm - genetics</subject><subject>signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Time Factors</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</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>eNp9kM1OwzAQhC0EoqVw4QGQL1yQUtZ2fo9QQQuqaEVBcLMcx0GGxIniVrRvj0NKe-NkrffbnZ1B6JzAkADQ67qp7JACS9gB6hNIIg_ADw5RH2gEnk9Y1EMn1n4COBzoMeqRMAY_jsM-WkxWpTC4EKU22ngBFibbVQRwqTItlirDH8oorNZ1o6zVlcFVjlvdpWtiKRqpTVUKLFVR2FN0lIvCqrPtO0Cv93cvo4k3nY0fRjdTT7IkYJ6KgCZJ5Ms8k9KPQhJnQUzzOBFZkubCT6X7EgFTqYRUkpQ4OzRVsjVKQIRsgK66vdIdYhuV87rRpWg2nABvk-Hthfw3GQdfdHC9Sp2pPbqNwgGXW0BYKYq8EUZqu-diQsEn4DjScd-6UJt_JPn8ebb4E_e6GW2Xar2bEc0XDyMWBfztacxvqf_-OJoHnLEfj7GKTw</recordid><startdate>20060915</startdate><enddate>20060915</enddate><creator>Calaluce, Robert</creator><creator>Beck, Shaleen K.</creator><creator>Bair, Elisabeth L.</creator><creator>Pandey, Ritu</creator><creator>Greer, Kevin A.</creator><creator>Hoying, Adam M.</creator><creator>Hoying, James B.</creator><creator>Mount, David W.</creator><creator>Nagle, Raymond B.</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></search><sort><creationdate>20060915</creationdate><title>Human laminin-5 and laminin-10 mediated gene expression of prostate carcinoma cells</title><author>Calaluce, Robert ; Beck, Shaleen K. ; Bair, Elisabeth L. ; Pandey, Ritu ; Greer, Kevin A. ; Hoying, Adam M. ; Hoying, James B. ; Mount, David W. ; Nagle, Raymond B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3953-e7029974cfdcc47618d582f89ad9bfa4bc618a53ebc0bc1b10272bec039310a63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Biological and medical sciences</topic><topic>Calpain - genetics</topic><topic>Calpain - metabolism</topic><topic>cDNA microarray</topic><topic>Cell Adhesion Molecules - physiology</topic><topic>Cell Line, Tumor</topic><topic>DNA, Neoplasm - genetics</topic><topic>ErbB Receptors - genetics</topic><topic>ErbB Receptors - metabolism</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Kalinin</topic><topic>Laminin - physiology</topic><topic>laminin-10</topic><topic>laminin-5</topic><topic>Male</topic><topic>Male genital diseases</topic><topic>MAP Kinase Signaling System - genetics</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>prostate carcinoma cells</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>RNA, Neoplasm - genetics</topic><topic>signal transduction</topic><topic>Signal Transduction - genetics</topic><topic>Time Factors</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>Calaluce, Robert</creatorcontrib><creatorcontrib>Beck, Shaleen K.</creatorcontrib><creatorcontrib>Bair, Elisabeth L.</creatorcontrib><creatorcontrib>Pandey, Ritu</creatorcontrib><creatorcontrib>Greer, Kevin A.</creatorcontrib><creatorcontrib>Hoying, Adam M.</creatorcontrib><creatorcontrib>Hoying, James B.</creatorcontrib><creatorcontrib>Mount, David W.</creatorcontrib><creatorcontrib>Nagle, Raymond B.</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><jtitle>The Prostate</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Calaluce, Robert</au><au>Beck, Shaleen K.</au><au>Bair, Elisabeth L.</au><au>Pandey, Ritu</au><au>Greer, Kevin A.</au><au>Hoying, Adam M.</au><au>Hoying, James B.</au><au>Mount, David W.</au><au>Nagle, Raymond B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human laminin-5 and laminin-10 mediated gene expression of prostate carcinoma cells</atitle><jtitle>The Prostate</jtitle><addtitle>Prostate</addtitle><date>2006-09-15</date><risdate>2006</risdate><volume>66</volume><issue>13</issue><spage>1381</spage><epage>1390</epage><pages>1381-1390</pages><issn>0270-4137</issn><eissn>1097-0045</eissn><coden>PRSTDS</coden><abstract>In prostate cancer progression, the basal lamina switches from predominantly laminin‐5 to laminin‐10. DU‐145 prostate cancer cells were treated with either soluble laminin‐5 (20 ng/ml) or laminin‐10 (1 µg/ml) for 6, 24, and 48 hr. Total RNA was harvested for a 7,500 human cDNA microarray. Hybridizations were carried out in accordance with a 10 sample analysis of variance (ANOVA) statistical model. One thousand one hundred sixteen genes had measurable expression 2 standard deviations above background and 50% of spots for any given sample for all hybridizations were positive. Expression values of significantly varying genes were clustered and a list of 408 genes (P < 0.05) with a 1.5 or greater fold change in at least one time point were chosen for further analysis. Seventy eight changed in a time‐dependent manner with laminin‐10 treatment, 85 changed with laminin‐5, and 13 showed changes with both treatments. The 408 genes that passed a paired t‐test in at least one time‐dependent category were further analyzed using Pathway Miner. One of the largest gene association networks involved signal transduction in the growth factor‐MAP kinase pathways. EGFR was validated by real‐time PCR and laminin‐10 mediated cell adhesion activated EGFR in DU‐145 cells. Both laminins appear to be important signal transducers in prostate cancer. Prostate 66: 1381–1390, 2006. © 2006 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>16804886</pmid><doi>10.1002/pros.20393</doi><tpages>10</tpages></addata></record> |
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| ispartof | The Prostate, 2006-09, Vol.66 (13), p.1381-1390 |
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| subjects | Biological and medical sciences Calpain - genetics Calpain - metabolism cDNA microarray Cell Adhesion Molecules - physiology Cell Line, Tumor DNA, Neoplasm - genetics ErbB Receptors - genetics ErbB Receptors - metabolism Gene Expression Profiling Gene Expression Regulation, Neoplastic - drug effects Gene Expression Regulation, Neoplastic - genetics Gynecology. Andrology. Obstetrics Humans Kalinin Laminin - physiology laminin-10 laminin-5 Male Male genital diseases MAP Kinase Signaling System - genetics Medical sciences Nephrology. Urinary tract diseases Oligonucleotide Array Sequence Analysis prostate carcinoma cells Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology RNA, Neoplasm - genetics signal transduction Signal Transduction - genetics Time Factors Tumors Tumors of the urinary system Urinary tract. Prostate gland |
| title | Human laminin-5 and laminin-10 mediated gene expression of prostate carcinoma cells |
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