Regulation of cysteinyl leukotriene receptor 2 expression--a potential anti-tumor mechanism
The cysteinyl leukotrienes receptors (CysLTRs) are implicated in many different pathological conditions, such as inflammation and cancer. We have previously shown that colon cancer patients with high CysLT(1)R and low CysLT(2)R expression demonstrate poor prognosis. Therefore, we wanted to investiga...
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| description | The cysteinyl leukotrienes receptors (CysLTRs) are implicated in many different pathological conditions, such as inflammation and cancer. We have previously shown that colon cancer patients with high CysLT(1)R and low CysLT(2)R expression demonstrate poor prognosis. Therefore, we wanted to investigate ways for the transcriptional regulation of CysLT(2)R, which still remains to be poorly understood.
We investigated the potential role of the anti-tumorigenic interferon α (IFN-α) and the mitogenic epidermal growth factor (EGF) on CysLT(2)R regulation using non-transformed intestinal epithelial cell lines and colon cancer cells to elucidate the effects on the CysLT(2)R expression and regulation. This was done using Western blot, qPCR, luciferase reporter assay and a colon cancer patient array. We found a binding site for the transcription factor IRF-7 in the putative promoter region of CysLT(2)R. This site was involved in the IFN-α induced activity of the CysLT(2)R luciferase reporter assay. In addition, IFN-α induced the activity of the differentiation marker alkaline phosphatase along with the expression of mucin-2, which protects the epithelial layer from damage. Interestingly, EGF suppressed both the expression and promoter activity of the CysLT(2)R. E-boxes present in the CysLT(2)R putative promoter region were involved in the suppressing effect. CysLT(2)R signaling was able to suppress cell migration that was induced by EGF signaling.
The patient array showed that aggressive tumors generally expressed less IFN-α receptor and more EGFR. Interestingly, there was a negative correlation between CysLT(2)R and EGFR expression. Our data strengthens the idea that there is a protective role against tumor progression for CysLT(2)R and that it highlights new possibilities to regulate the CysLT(2)R. |
| doi_str_mv | 10.1371/journal.pone.0029060 |
| format | Article |
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We investigated the potential role of the anti-tumorigenic interferon α (IFN-α) and the mitogenic epidermal growth factor (EGF) on CysLT(2)R regulation using non-transformed intestinal epithelial cell lines and colon cancer cells to elucidate the effects on the CysLT(2)R expression and regulation. This was done using Western blot, qPCR, luciferase reporter assay and a colon cancer patient array. We found a binding site for the transcription factor IRF-7 in the putative promoter region of CysLT(2)R. This site was involved in the IFN-α induced activity of the CysLT(2)R luciferase reporter assay. In addition, IFN-α induced the activity of the differentiation marker alkaline phosphatase along with the expression of mucin-2, which protects the epithelial layer from damage. Interestingly, EGF suppressed both the expression and promoter activity of the CysLT(2)R. E-boxes present in the CysLT(2)R putative promoter region were involved in the suppressing effect. CysLT(2)R signaling was able to suppress cell migration that was induced by EGF signaling.
The patient array showed that aggressive tumors generally expressed less IFN-α receptor and more EGFR. Interestingly, there was a negative correlation between CysLT(2)R and EGFR expression. Our data strengthens the idea that there is a protective role against tumor progression for CysLT(2)R and that it highlights new possibilities to regulate the CysLT(2)R.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0029060</identifier><identifier>PMID: 22194989</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alkaline phosphatase ; Base Sequence ; Binding Sites ; Biological response modifiers ; Biology ; Caco-2 Cells ; Cancer ; Cancer and Oncology ; Cancer och onkologi ; Cell Differentiation - drug effects ; Cell growth ; Cell migration ; Chemokines ; Clinical Medicine ; Colon ; Colon cancer ; Colorectal cancer ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Cytokines ; E-Box Elements - genetics ; Epidermal growth factor ; Epidermal Growth Factor - pharmacology ; Epidermal growth factor receptors ; Epidermal growth factors ; Epithelial cells ; Gastroenterology ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Gene regulation ; Genes, Reporter - genetics ; Hospitals ; Humans ; Immunoglobulins ; Inflammation ; Inflammatory bowel disease ; Interferon ; Interferon regulatory factor 7 ; Interferon Regulatory Factor-7 - metabolism ; Interferon-alpha - pharmacology ; Intestine ; Klinisk medicin ; Laboratories ; Leukotrienes ; Luciferase ; Luciferases - metabolism ; Medical and Health Sciences ; Medicin och hälsovetenskap ; Medicine ; Molecular Sequence Data ; Mucin ; Pathology ; Phosphatases ; Prognosis ; Promoter Regions, Genetic - genetics ; Receptor, Epidermal Growth Factor - metabolism ; Receptors ; Receptors, Leukotriene - genetics ; Receptors, Leukotriene - metabolism ; Signal Transduction - drug effects ; Signaling ; Snail Family Transcription Factors ; Transcription Factors - metabolism ; Tumor cell lines ; Tumors</subject><ispartof>PloS one, 2011-12, Vol.6 (12), p.e29060</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Magnusson et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Magnusson et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c760t-980caebde4dbdfe620708e77c8b45a53dd41e6f8e8096886b33766c5ca54cc053</citedby><cites>FETCH-LOGICAL-c760t-980caebde4dbdfe620708e77c8b45a53dd41e6f8e8096886b33766c5ca54cc053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240642/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240642/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,552,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22194989$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://lup.lub.lu.se/record/2273580$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><contributor>Bozza, Patricia T.</contributor><creatorcontrib>Magnusson, Cecilia</creatorcontrib><creatorcontrib>Bengtsson, Astrid M</creatorcontrib><creatorcontrib>Liu, Minghui</creatorcontrib><creatorcontrib>Liu, Jian</creatorcontrib><creatorcontrib>Ceder, Yvonne</creatorcontrib><creatorcontrib>Ehrnström, Roy</creatorcontrib><creatorcontrib>Sjölander, Anita</creatorcontrib><title>Regulation of cysteinyl leukotriene receptor 2 expression--a potential anti-tumor mechanism</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The cysteinyl leukotrienes receptors (CysLTRs) are implicated in many different pathological conditions, such as inflammation and cancer. We have previously shown that colon cancer patients with high CysLT(1)R and low CysLT(2)R expression demonstrate poor prognosis. Therefore, we wanted to investigate ways for the transcriptional regulation of CysLT(2)R, which still remains to be poorly understood.
We investigated the potential role of the anti-tumorigenic interferon α (IFN-α) and the mitogenic epidermal growth factor (EGF) on CysLT(2)R regulation using non-transformed intestinal epithelial cell lines and colon cancer cells to elucidate the effects on the CysLT(2)R expression and regulation. This was done using Western blot, qPCR, luciferase reporter assay and a colon cancer patient array. We found a binding site for the transcription factor IRF-7 in the putative promoter region of CysLT(2)R. This site was involved in the IFN-α induced activity of the CysLT(2)R luciferase reporter assay. In addition, IFN-α induced the activity of the differentiation marker alkaline phosphatase along with the expression of mucin-2, which protects the epithelial layer from damage. Interestingly, EGF suppressed both the expression and promoter activity of the CysLT(2)R. E-boxes present in the CysLT(2)R putative promoter region were involved in the suppressing effect. CysLT(2)R signaling was able to suppress cell migration that was induced by EGF signaling.
The patient array showed that aggressive tumors generally expressed less IFN-α receptor and more EGFR. Interestingly, there was a negative correlation between CysLT(2)R and EGFR expression. Our data strengthens the idea that there is a protective role against tumor progression for CysLT(2)R and that it highlights new possibilities to regulate the CysLT(2)R.</description><subject>Alkaline phosphatase</subject><subject>Base Sequence</subject><subject>Binding Sites</subject><subject>Biological response modifiers</subject><subject>Biology</subject><subject>Caco-2 Cells</subject><subject>Cancer</subject><subject>Cancer and Oncology</subject><subject>Cancer och onkologi</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Chemokines</subject><subject>Clinical Medicine</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Cytokines</subject><subject>E-Box Elements - genetics</subject><subject>Epidermal growth factor</subject><subject>Epidermal Growth Factor - pharmacology</subject><subject>Epidermal growth factor receptors</subject><subject>Epidermal growth factors</subject><subject>Epithelial cells</subject><subject>Gastroenterology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene regulation</subject><subject>Genes, Reporter - genetics</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Inflammation</subject><subject>Inflammatory bowel disease</subject><subject>Interferon</subject><subject>Interferon regulatory factor 7</subject><subject>Interferon Regulatory Factor-7 - metabolism</subject><subject>Interferon-alpha - pharmacology</subject><subject>Intestine</subject><subject>Klinisk medicin</subject><subject>Laboratories</subject><subject>Leukotrienes</subject><subject>Luciferase</subject><subject>Luciferases - metabolism</subject><subject>Medical and Health Sciences</subject><subject>Medicin och hälsovetenskap</subject><subject>Medicine</subject><subject>Molecular Sequence Data</subject><subject>Mucin</subject><subject>Pathology</subject><subject>Phosphatases</subject><subject>Prognosis</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>Receptors</subject><subject>Receptors, Leukotriene - genetics</subject><subject>Receptors, Leukotriene - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Snail Family Transcription Factors</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>D8T</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7rr6D0QLguBFx3y0SXojLIsfAwML68eNFyFJT2eytk03SXXn35txZpcpKEgIKclz3p7zJifLnmO0wJTjt9du8oPqFqMbYIEQqRFDD7JTXFNSMILow6Pvk-xJCNcIVVQw9jg7IQTXZS3q0-z7FaynTkXrhty1udmGCHbYdnkH0w8XvYUBcg8Gxuh8TnK4HT2EkPCiUPnoIgzRqi5XaSni1CeoB7NRgw390-xRq7oAzw7rWfb1w_svF5-K1eXH5cX5qjCcoVjUAhkFuoGy0U0LKV-OBHBuhC4rVdGmKTGwVoBANROCaUo5Y6YyqiqNSTWdZS_3umPngjz4EiSmmGDOMMaJWO6JxqlrOXrbK7-VTln5Z8P5tVQ-WtOBRIbjtmwp5giVqgGtcKURKFIbWqcfJ63VXiv8gnHSM7VuGtPUacoAkqRbIRop2WquZUk4l5oQJneVcGKE0LBL_t0h-Un30Jjkp1fdTHV-MtiNXLufkpISsZIkgVcHAe9uJgjxHw4cqLVKRdqhTXerTG-DkeclZ4IhXNWJWvyFSqOB3pr00Fqb9mcBb2YBiYlwG9dqCkEuP1_9P3v5bc6-PmI3oLq4Ca6bdu80zMFyDxrvQvDQ3juHkdz1yZ0bctcn8tAnKezFsev3QXeNQX8DswEOIw</recordid><startdate>20111215</startdate><enddate>20111215</enddate><creator>Magnusson, Cecilia</creator><creator>Bengtsson, Astrid M</creator><creator>Liu, Minghui</creator><creator>Liu, Jian</creator><creator>Ceder, Yvonne</creator><creator>Ehrnström, Roy</creator><creator>Sjölander, Anita</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AGCHP</scope><scope>AOWAS</scope><scope>D8T</scope><scope>D95</scope><scope>ZZAVC</scope><scope>DOA</scope></search><sort><creationdate>20111215</creationdate><title>Regulation of cysteinyl leukotriene receptor 2 expression--a potential anti-tumor mechanism</title><author>Magnusson, Cecilia ; Bengtsson, Astrid M ; Liu, Minghui ; Liu, Jian ; Ceder, Yvonne ; Ehrnström, Roy ; Sjölander, Anita</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c760t-980caebde4dbdfe620708e77c8b45a53dd41e6f8e8096886b33766c5ca54cc053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Alkaline phosphatase</topic><topic>Base Sequence</topic><topic>Binding Sites</topic><topic>Biological response modifiers</topic><topic>Biology</topic><topic>Caco-2 Cells</topic><topic>Cancer</topic><topic>Cancer and Oncology</topic><topic>Cancer och onkologi</topic><topic>Cell Differentiation - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SWEPUB Lunds universitet full text</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Lunds universitet</collection><collection>SwePub Articles full text</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Magnusson, Cecilia</au><au>Bengtsson, Astrid M</au><au>Liu, Minghui</au><au>Liu, Jian</au><au>Ceder, Yvonne</au><au>Ehrnström, Roy</au><au>Sjölander, Anita</au><au>Bozza, Patricia T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of cysteinyl leukotriene receptor 2 expression--a potential anti-tumor mechanism</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-12-15</date><risdate>2011</risdate><volume>6</volume><issue>12</issue><spage>e29060</spage><pages>e29060-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The cysteinyl leukotrienes receptors (CysLTRs) are implicated in many different pathological conditions, such as inflammation and cancer. We have previously shown that colon cancer patients with high CysLT(1)R and low CysLT(2)R expression demonstrate poor prognosis. Therefore, we wanted to investigate ways for the transcriptional regulation of CysLT(2)R, which still remains to be poorly understood.
We investigated the potential role of the anti-tumorigenic interferon α (IFN-α) and the mitogenic epidermal growth factor (EGF) on CysLT(2)R regulation using non-transformed intestinal epithelial cell lines and colon cancer cells to elucidate the effects on the CysLT(2)R expression and regulation. This was done using Western blot, qPCR, luciferase reporter assay and a colon cancer patient array. We found a binding site for the transcription factor IRF-7 in the putative promoter region of CysLT(2)R. This site was involved in the IFN-α induced activity of the CysLT(2)R luciferase reporter assay. In addition, IFN-α induced the activity of the differentiation marker alkaline phosphatase along with the expression of mucin-2, which protects the epithelial layer from damage. Interestingly, EGF suppressed both the expression and promoter activity of the CysLT(2)R. E-boxes present in the CysLT(2)R putative promoter region were involved in the suppressing effect. CysLT(2)R signaling was able to suppress cell migration that was induced by EGF signaling.
The patient array showed that aggressive tumors generally expressed less IFN-α receptor and more EGFR. Interestingly, there was a negative correlation between CysLT(2)R and EGFR expression. Our data strengthens the idea that there is a protective role against tumor progression for CysLT(2)R and that it highlights new possibilities to regulate the CysLT(2)R.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22194989</pmid><doi>10.1371/journal.pone.0029060</doi><tpages>e29060</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2011-12, Vol.6 (12), p.e29060 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1312176111 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; SWEPUB Freely available online; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Alkaline phosphatase Base Sequence Binding Sites Biological response modifiers Biology Caco-2 Cells Cancer Cancer and Oncology Cancer och onkologi Cell Differentiation - drug effects Cell growth Cell migration Chemokines Clinical Medicine Colon Colon cancer Colorectal cancer Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Cytokines E-Box Elements - genetics Epidermal growth factor Epidermal Growth Factor - pharmacology Epidermal growth factor receptors Epidermal growth factors Epithelial cells Gastroenterology Gene expression Gene Expression Regulation, Neoplastic - drug effects Gene regulation Genes, Reporter - genetics Hospitals Humans Immunoglobulins Inflammation Inflammatory bowel disease Interferon Interferon regulatory factor 7 Interferon Regulatory Factor-7 - metabolism Interferon-alpha - pharmacology Intestine Klinisk medicin Laboratories Leukotrienes Luciferase Luciferases - metabolism Medical and Health Sciences Medicin och hälsovetenskap Medicine Molecular Sequence Data Mucin Pathology Phosphatases Prognosis Promoter Regions, Genetic - genetics Receptor, Epidermal Growth Factor - metabolism Receptors Receptors, Leukotriene - genetics Receptors, Leukotriene - metabolism Signal Transduction - drug effects Signaling Snail Family Transcription Factors Transcription Factors - metabolism Tumor cell lines Tumors |
| title | Regulation of cysteinyl leukotriene receptor 2 expression--a potential anti-tumor mechanism |
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