Kallikrein-related peptidase signaling in colon carcinoma cells: targeting proteinase-activated receptors
We hypothesized that kallikrein-related peptidase 14 (KLK14) is produced by colonic tumors and can promote tumorigenesis by activating proteinase-activated receptors (PARs). We found that KLK14 is expressed in human colon adenocarcinoma cells but not in adjacent cancer-free tissue; KLK14 mRNA, prese...
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| Veröffentlicht in: | Biological chemistry 2012-05, Vol.393 (5), p.413-420 |
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| creator | Chung, Hyunjae Hamza, Magda Oikonomopoulou, Katerina Gratio, Valérie Saifeddine, Mahmoud Virca, G. Duke Diamandis, Eleftherios P. Hollenberg, Morley D. Darmoul, Dalila |
| description | We hypothesized that kallikrein-related peptidase 14 (KLK14) is produced by colonic tumors and can promote tumorigenesis by activating proteinase-activated receptors (PARs). We found that KLK14 is expressed in human colon adenocarcinoma cells but not in adjacent cancer-free tissue; KLK14 mRNA, present in colon cancer, leads to KLK14 protein expression and secretion; and KLK14 signals viaPAR-2 in HT-29 cells to cause (1) receptor activation/internalization, (2) increases in intracellular calcium, (3) stimulation of ERK1/2/MAP kinase phosphorylation, and (4) cell proliferation. We suggest that KLK14, acting via PAR-2, represents an autocrine/paracrine regulator of colon tumorigenesis. |
| doi_str_mv | 10.1515/bc-2011-231 |
| format | Article |
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Duke ; Diamandis, Eleftherios P. ; Hollenberg, Morley D. ; Darmoul, Dalila</creator><creatorcontrib>Chung, Hyunjae ; Hamza, Magda ; Oikonomopoulou, Katerina ; Gratio, Valérie ; Saifeddine, Mahmoud ; Virca, G. Duke ; Diamandis, Eleftherios P. ; Hollenberg, Morley D. ; Darmoul, Dalila</creatorcontrib><description>We hypothesized that kallikrein-related peptidase 14 (KLK14) is produced by colonic tumors and can promote tumorigenesis by activating proteinase-activated receptors (PARs). We found that KLK14 is expressed in human colon adenocarcinoma cells but not in adjacent cancer-free tissue; KLK14 mRNA, present in colon cancer, leads to KLK14 protein expression and secretion; and KLK14 signals viaPAR-2 in HT-29 cells to cause (1) receptor activation/internalization, (2) increases in intracellular calcium, (3) stimulation of ERK1/2/MAP kinase phosphorylation, and (4) cell proliferation. We suggest that KLK14, acting via PAR-2, represents an autocrine/paracrine regulator of colon tumorigenesis.</description><identifier>ISSN: 1431-6730</identifier><identifier>EISSN: 1437-4315</identifier><identifier>DOI: 10.1515/bc-2011-231</identifier><identifier>PMID: 22505523</identifier><language>eng</language><publisher>Germany: Walter de Gruyter</publisher><subject>cancer ; colon ; Colonic Neoplasms - enzymology ; Colonic Neoplasms - genetics ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Gene Expression Regulation, Neoplastic ; HT29 Cells ; Humans ; kallikrein ; Kallikreins - genetics ; Kallikreins - metabolism ; PARs ; proliferation ; Protein Binding ; Receptor, PAR-2 - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal Transduction ; signaling</subject><ispartof>Biological chemistry, 2012-05, Vol.393 (5), p.413-420</ispartof><rights>2012 by Walter de Gruyter Berlin Boston</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-974b4a741b1defe5d409a16ac964b0de1c2a52371d7e8abd4d13464c339e540a3</citedby><cites>FETCH-LOGICAL-c444t-974b4a741b1defe5d409a16ac964b0de1c2a52371d7e8abd4d13464c339e540a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.degruyter.com/document/doi/10.1515/bc-2011-231/pdf$$EPDF$$P50$$Gwalterdegruyter$$H</linktopdf><linktohtml>$$Uhttps://www.degruyter.com/document/doi/10.1515/bc-2011-231/html$$EHTML$$P50$$Gwalterdegruyter$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,66759,68543</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22505523$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chung, Hyunjae</creatorcontrib><creatorcontrib>Hamza, Magda</creatorcontrib><creatorcontrib>Oikonomopoulou, Katerina</creatorcontrib><creatorcontrib>Gratio, Valérie</creatorcontrib><creatorcontrib>Saifeddine, Mahmoud</creatorcontrib><creatorcontrib>Virca, G. Duke</creatorcontrib><creatorcontrib>Diamandis, Eleftherios P.</creatorcontrib><creatorcontrib>Hollenberg, Morley D.</creatorcontrib><creatorcontrib>Darmoul, Dalila</creatorcontrib><title>Kallikrein-related peptidase signaling in colon carcinoma cells: targeting proteinase-activated receptors</title><title>Biological chemistry</title><addtitle>Biol Chem</addtitle><description>We hypothesized that kallikrein-related peptidase 14 (KLK14) is produced by colonic tumors and can promote tumorigenesis by activating proteinase-activated receptors (PARs). We found that KLK14 is expressed in human colon adenocarcinoma cells but not in adjacent cancer-free tissue; KLK14 mRNA, present in colon cancer, leads to KLK14 protein expression and secretion; and KLK14 signals viaPAR-2 in HT-29 cells to cause (1) receptor activation/internalization, (2) increases in intracellular calcium, (3) stimulation of ERK1/2/MAP kinase phosphorylation, and (4) cell proliferation. We suggest that KLK14, acting via PAR-2, represents an autocrine/paracrine regulator of colon tumorigenesis.</description><subject>cancer</subject><subject>colon</subject><subject>Colonic Neoplasms - enzymology</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>kallikrein</subject><subject>Kallikreins - genetics</subject><subject>Kallikreins - metabolism</subject><subject>PARs</subject><subject>proliferation</subject><subject>Protein Binding</subject><subject>Receptor, PAR-2 - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction</subject><subject>signaling</subject><issn>1431-6730</issn><issn>1437-4315</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkcFPFTEQhxujEURP3s0eTUy1s213KTeDCgrGmGA8NrPtvJdC3-6j7Qr893Z5yMlLO4fv92XyG8Zeg3gPGvSHwfFWAPBWwhO2D0r2XEnQT-9n4F0vxR57kfOlEOJQKPmc7bWtFlq3cp-FM4wxXCUKI08UsZBvtrQtwWOmJof1iDGM6yaMjZviVF9MLozTBhtHMeajpmBaU1mYbZpK9dQgR1fCn3tZIld1U8ov2bMVxkyvHv4D9uvL54vjU37-4-Tr8cdz7pRShZteDQp7BQN4WpH2ShiEDp3p1CA8gWuxbt6D7-kQB688SNUpJ6UhrQTKA_Z2563rXM-Ui92EvOyKI01ztiAEmK41Rlb03Q51aco50cpuU9hguquQXbq1g7NLt7Z2W-k3D-J52JB_ZP-VWYGjHXCDsVDytE7zXR3s5TSn2mP-r9ZIrWAJ81045EK3j3JMV7ZesNf254Wy383Jp2-nv8-sln8BxAeYDw</recordid><startdate>20120501</startdate><enddate>20120501</enddate><creator>Chung, Hyunjae</creator><creator>Hamza, Magda</creator><creator>Oikonomopoulou, Katerina</creator><creator>Gratio, Valérie</creator><creator>Saifeddine, Mahmoud</creator><creator>Virca, G. Duke</creator><creator>Diamandis, Eleftherios P.</creator><creator>Hollenberg, Morley D.</creator><creator>Darmoul, Dalila</creator><general>Walter de Gruyter</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></search><sort><creationdate>20120501</creationdate><title>Kallikrein-related peptidase signaling in colon carcinoma cells: targeting proteinase-activated receptors</title><author>Chung, Hyunjae ; Hamza, Magda ; Oikonomopoulou, Katerina ; Gratio, Valérie ; Saifeddine, Mahmoud ; Virca, G. Duke ; Diamandis, Eleftherios P. ; Hollenberg, Morley D. ; Darmoul, Dalila</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-974b4a741b1defe5d409a16ac964b0de1c2a52371d7e8abd4d13464c339e540a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>cancer</topic><topic>colon</topic><topic>Colonic Neoplasms - enzymology</topic><topic>Colonic Neoplasms - genetics</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colonic Neoplasms - pathology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>HT29 Cells</topic><topic>Humans</topic><topic>kallikrein</topic><topic>Kallikreins - genetics</topic><topic>Kallikreins - metabolism</topic><topic>PARs</topic><topic>proliferation</topic><topic>Protein Binding</topic><topic>Receptor, PAR-2 - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction</topic><topic>signaling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chung, Hyunjae</creatorcontrib><creatorcontrib>Hamza, Magda</creatorcontrib><creatorcontrib>Oikonomopoulou, Katerina</creatorcontrib><creatorcontrib>Gratio, Valérie</creatorcontrib><creatorcontrib>Saifeddine, Mahmoud</creatorcontrib><creatorcontrib>Virca, G. Duke</creatorcontrib><creatorcontrib>Diamandis, Eleftherios P.</creatorcontrib><creatorcontrib>Hollenberg, Morley D.</creatorcontrib><creatorcontrib>Darmoul, Dalila</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><jtitle>Biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chung, Hyunjae</au><au>Hamza, Magda</au><au>Oikonomopoulou, Katerina</au><au>Gratio, Valérie</au><au>Saifeddine, Mahmoud</au><au>Virca, G. Duke</au><au>Diamandis, Eleftherios P.</au><au>Hollenberg, Morley D.</au><au>Darmoul, Dalila</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Kallikrein-related peptidase signaling in colon carcinoma cells: targeting proteinase-activated receptors</atitle><jtitle>Biological chemistry</jtitle><addtitle>Biol Chem</addtitle><date>2012-05-01</date><risdate>2012</risdate><volume>393</volume><issue>5</issue><spage>413</spage><epage>420</epage><pages>413-420</pages><issn>1431-6730</issn><eissn>1437-4315</eissn><abstract>We hypothesized that kallikrein-related peptidase 14 (KLK14) is produced by colonic tumors and can promote tumorigenesis by activating proteinase-activated receptors (PARs). We found that KLK14 is expressed in human colon adenocarcinoma cells but not in adjacent cancer-free tissue; KLK14 mRNA, present in colon cancer, leads to KLK14 protein expression and secretion; and KLK14 signals viaPAR-2 in HT-29 cells to cause (1) receptor activation/internalization, (2) increases in intracellular calcium, (3) stimulation of ERK1/2/MAP kinase phosphorylation, and (4) cell proliferation. We suggest that KLK14, acting via PAR-2, represents an autocrine/paracrine regulator of colon tumorigenesis.</abstract><cop>Germany</cop><pub>Walter de Gruyter</pub><pmid>22505523</pmid><doi>10.1515/bc-2011-231</doi><tpages>8</tpages></addata></record> |
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| ispartof | Biological chemistry, 2012-05, Vol.393 (5), p.413-420 |
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| source | MEDLINE; De Gruyter journals |
| subjects | cancer colon Colonic Neoplasms - enzymology Colonic Neoplasms - genetics Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Gene Expression Regulation, Neoplastic HT29 Cells Humans kallikrein Kallikreins - genetics Kallikreins - metabolism PARs proliferation Protein Binding Receptor, PAR-2 - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Signal Transduction signaling |
| title | Kallikrein-related peptidase signaling in colon carcinoma cells: targeting proteinase-activated receptors |
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