Kallikreins are involved in an miRNA network that contributes to prostate cancer progression
MicroRNAs (miRNAs) are short RNA nucleotides that negatively regulate their target genes. They are differentially expressed in prostate cancer. Kallikreins are genes that encode serine proteases and are dysregulated in cancer. We elucidated a miRNA-kallikrein network that can be involved in prostate...
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Veröffentlicht in: | Biological chemistry 2014-09, Vol.395 (9), p.991-1001 |
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creator | Samaan, Sara Lichner, Zsuzsanna Ding, Qiang Saleh, Carol Samuel, Joseph Streutker, Catherine Yousef, George M. |
description | MicroRNAs (miRNAs) are short RNA nucleotides that negatively regulate their target genes. They are differentially expressed in prostate cancer. Kallikreins are genes that encode serine proteases and are dysregulated in cancer. We elucidated a miRNA-kallikrein network that can be involved in prostate cancer progression. Target prediction identified 23 miRNAs that are dysregulated between high and low risk biochemical failure and are predicted to target five kallikreins linked to prostate cancer;
,
,
,
and
. We also identified 14 miRNAs that are differentially expressed between Gleason grades and are predicted to target these kallikreins. This demonstrates that kallikreins are downstream effectors through which miRNAs influence tumor progression. We show, through
and experimental analysis, that miR-378/422a and its gene targets
,
,
,
and
form an integrated circuit in prostate cancer. Our analysis shows that a minisatellite sequence in the kallikrein locus consists of a number of microsatellite repeats that represent predicted miRNA response elements. A number of kallikrein and non-kallikrein prostate cancer-related genes share these microsatellite repeats. We validated some of these interactions in prostate cancer cell lines. Finally, we provide preliminary evidence on the presence of a miRNA-mediated cross-talk between kallikreins, including a kallikrein pseudogene. |
doi_str_mv | 10.1515/hsz-2013-0288 |
format | Article |
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,
,
,
and
. We also identified 14 miRNAs that are differentially expressed between Gleason grades and are predicted to target these kallikreins. This demonstrates that kallikreins are downstream effectors through which miRNAs influence tumor progression. We show, through
and experimental analysis, that miR-378/422a and its gene targets
,
,
,
and
form an integrated circuit in prostate cancer. Our analysis shows that a minisatellite sequence in the kallikrein locus consists of a number of microsatellite repeats that represent predicted miRNA response elements. A number of kallikrein and non-kallikrein prostate cancer-related genes share these microsatellite repeats. We validated some of these interactions in prostate cancer cell lines. Finally, we provide preliminary evidence on the presence of a miRNA-mediated cross-talk between kallikreins, including a kallikrein pseudogene.</description><identifier>ISSN: 1431-6730</identifier><identifier>EISSN: 1437-4315</identifier><identifier>DOI: 10.1515/hsz-2013-0288</identifier><identifier>PMID: 25153383</identifier><language>eng</language><publisher>Germany: De Gruyter</publisher><subject>Base Sequence ; biochemical failure ; Disease Progression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Gleason grade ; Humans ; Kallikreins - metabolism ; Male ; MicroRNAs - genetics ; MicroRNAs - metabolism ; microsatellite repeat ; Minisatellite Repeats - genetics ; Models, Biological ; Molecular Sequence Data ; Neoplasm Grading ; personalized medicine ; prostate-specific antigen ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - pathology ; tumor markers</subject><ispartof>Biological chemistry, 2014-09, Vol.395 (9), p.991-1001</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c379t-ed446705e5322cc17c5132d97814fe8671f0f127c06511a6aad313745ddd8ea73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.degruyter.com/document/doi/10.1515/hsz-2013-0288/pdf$$EPDF$$P50$$Gwalterdegruyter$$H</linktopdf><linktohtml>$$Uhttps://www.degruyter.com/document/doi/10.1515/hsz-2013-0288/html$$EHTML$$P50$$Gwalterdegruyter$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,66497,68281</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25153383$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Samaan, Sara</creatorcontrib><creatorcontrib>Lichner, Zsuzsanna</creatorcontrib><creatorcontrib>Ding, Qiang</creatorcontrib><creatorcontrib>Saleh, Carol</creatorcontrib><creatorcontrib>Samuel, Joseph</creatorcontrib><creatorcontrib>Streutker, Catherine</creatorcontrib><creatorcontrib>Yousef, George M.</creatorcontrib><title>Kallikreins are involved in an miRNA network that contributes to prostate cancer progression</title><title>Biological chemistry</title><addtitle>Biol Chem</addtitle><description>MicroRNAs (miRNAs) are short RNA nucleotides that negatively regulate their target genes. They are differentially expressed in prostate cancer. Kallikreins are genes that encode serine proteases and are dysregulated in cancer. We elucidated a miRNA-kallikrein network that can be involved in prostate cancer progression. Target prediction identified 23 miRNAs that are dysregulated between high and low risk biochemical failure and are predicted to target five kallikreins linked to prostate cancer;
,
,
,
and
. We also identified 14 miRNAs that are differentially expressed between Gleason grades and are predicted to target these kallikreins. This demonstrates that kallikreins are downstream effectors through which miRNAs influence tumor progression. We show, through
and experimental analysis, that miR-378/422a and its gene targets
,
,
,
and
form an integrated circuit in prostate cancer. Our analysis shows that a minisatellite sequence in the kallikrein locus consists of a number of microsatellite repeats that represent predicted miRNA response elements. A number of kallikrein and non-kallikrein prostate cancer-related genes share these microsatellite repeats. We validated some of these interactions in prostate cancer cell lines. Finally, we provide preliminary evidence on the presence of a miRNA-mediated cross-talk between kallikreins, including a kallikrein pseudogene.</description><subject>Base Sequence</subject><subject>biochemical failure</subject><subject>Disease Progression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Regulatory Networks</subject><subject>Gleason grade</subject><subject>Humans</subject><subject>Kallikreins - metabolism</subject><subject>Male</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>microsatellite repeat</subject><subject>Minisatellite Repeats - genetics</subject><subject>Models, Biological</subject><subject>Molecular Sequence Data</subject><subject>Neoplasm Grading</subject><subject>personalized medicine</subject><subject>prostate-specific antigen</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>tumor markers</subject><issn>1431-6730</issn><issn>1437-4315</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM9LHDEUx4NY6o_26LXk6GXavGQyyUAvImqlYkHsrRCyyZt13NnMmmQU_evNdtWbeMo38Hnfx_sQcgDsO0iQP27SU8UZiIpxrbfILtRCVbUAuf0_Q9UowXbIXkq3jDHNavGZ7PAyKYQWu-TfbzsM_SJiHxK1EWkf7sfhHn0J1Aa67K8uj2jA_DDGBc03NlM3hhz72ZQx0TzSVRxTthmps8FhXP_nEVPqx_CFfOrskPDry7tP_p6eXB__qi7-nJ0fH11UTqg2V-jrulFMohScOwfKSRDct0pD3aFuFHSsA64caySAbaz1AoSqpfdeo1VinxxuesvuuwlTNss-ORwGG3CckgHFVWnRnH-MSqmYrpVoC1ptUFcuTBE7s4r90sZHA8ys3Zvi3qzdm7X7wn97qZ5mS_Rv9KvsAvzcAA92yBg9zuP0WIK5HacYiqB3ilvZti2IZ6fjkyk</recordid><startdate>20140901</startdate><enddate>20140901</enddate><creator>Samaan, Sara</creator><creator>Lichner, Zsuzsanna</creator><creator>Ding, Qiang</creator><creator>Saleh, Carol</creator><creator>Samuel, Joseph</creator><creator>Streutker, Catherine</creator><creator>Yousef, George M.</creator><general>De Gruyter</general><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>7TM</scope></search><sort><creationdate>20140901</creationdate><title>Kallikreins are involved in an miRNA network that contributes to prostate cancer progression</title><author>Samaan, Sara ; Lichner, Zsuzsanna ; Ding, Qiang ; Saleh, Carol ; Samuel, Joseph ; Streutker, Catherine ; Yousef, George M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c379t-ed446705e5322cc17c5132d97814fe8671f0f127c06511a6aad313745ddd8ea73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Base Sequence</topic><topic>biochemical failure</topic><topic>Disease Progression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Regulatory Networks</topic><topic>Gleason grade</topic><topic>Humans</topic><topic>Kallikreins - metabolism</topic><topic>Male</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>microsatellite repeat</topic><topic>Minisatellite Repeats - genetics</topic><topic>Models, Biological</topic><topic>Molecular Sequence Data</topic><topic>Neoplasm Grading</topic><topic>personalized medicine</topic><topic>prostate-specific antigen</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - pathology</topic><topic>tumor markers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Samaan, Sara</creatorcontrib><creatorcontrib>Lichner, Zsuzsanna</creatorcontrib><creatorcontrib>Ding, Qiang</creatorcontrib><creatorcontrib>Saleh, Carol</creatorcontrib><creatorcontrib>Samuel, Joseph</creatorcontrib><creatorcontrib>Streutker, Catherine</creatorcontrib><creatorcontrib>Yousef, George M.</creatorcontrib><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>Nucleic Acids Abstracts</collection><jtitle>Biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Samaan, Sara</au><au>Lichner, Zsuzsanna</au><au>Ding, Qiang</au><au>Saleh, Carol</au><au>Samuel, Joseph</au><au>Streutker, Catherine</au><au>Yousef, George M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Kallikreins are involved in an miRNA network that contributes to prostate cancer progression</atitle><jtitle>Biological chemistry</jtitle><addtitle>Biol Chem</addtitle><date>2014-09-01</date><risdate>2014</risdate><volume>395</volume><issue>9</issue><spage>991</spage><epage>1001</epage><pages>991-1001</pages><issn>1431-6730</issn><eissn>1437-4315</eissn><abstract>MicroRNAs (miRNAs) are short RNA nucleotides that negatively regulate their target genes. They are differentially expressed in prostate cancer. Kallikreins are genes that encode serine proteases and are dysregulated in cancer. We elucidated a miRNA-kallikrein network that can be involved in prostate cancer progression. Target prediction identified 23 miRNAs that are dysregulated between high and low risk biochemical failure and are predicted to target five kallikreins linked to prostate cancer;
,
,
,
and
. We also identified 14 miRNAs that are differentially expressed between Gleason grades and are predicted to target these kallikreins. This demonstrates that kallikreins are downstream effectors through which miRNAs influence tumor progression. We show, through
and experimental analysis, that miR-378/422a and its gene targets
,
,
,
and
form an integrated circuit in prostate cancer. Our analysis shows that a minisatellite sequence in the kallikrein locus consists of a number of microsatellite repeats that represent predicted miRNA response elements. A number of kallikrein and non-kallikrein prostate cancer-related genes share these microsatellite repeats. We validated some of these interactions in prostate cancer cell lines. Finally, we provide preliminary evidence on the presence of a miRNA-mediated cross-talk between kallikreins, including a kallikrein pseudogene.</abstract><cop>Germany</cop><pub>De Gruyter</pub><pmid>25153383</pmid><doi>10.1515/hsz-2013-0288</doi><tpages>11</tpages></addata></record> |
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subjects | Base Sequence biochemical failure Disease Progression Gene Expression Profiling Gene Expression Regulation, Neoplastic Gene Regulatory Networks Gleason grade Humans Kallikreins - metabolism Male MicroRNAs - genetics MicroRNAs - metabolism microsatellite repeat Minisatellite Repeats - genetics Models, Biological Molecular Sequence Data Neoplasm Grading personalized medicine prostate-specific antigen Prostatic Neoplasms - genetics Prostatic Neoplasms - pathology tumor markers |
title | Kallikreins are involved in an miRNA network that contributes to prostate cancer progression |
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