MicroRNA-155 Regulates Inflammatory Cytokine Production in Tumor-associated Macrophages via Targeting C/EBPβ
Macrophages （Mφ） are prominent components of solid tumors and exhibit distinct phenotypes in different microenvironments. We have recently found that tumors can alter the normal developmental process of Mφ to trigger transient activation of monocytes, but the underlying regulatory mechanisms are inc...
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| Veröffentlicht in: | Cellular & molecular immunology 2009-10, Vol.6 (5), p.343-352 |
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| creator | He, Min Xu, Zhenqun Ding, Tong Kuang, Dong-Ming Zheng, Limin |
| description | Macrophages （Mφ） are prominent components of solid tumors and exhibit distinct phenotypes in different microenvironments. We have recently found that tumors can alter the normal developmental process of Mφ to trigger transient activation of monocytes, but the underlying regulatory mechanisms are incompletely understood. Here, we showed that the protein expression of transcription factor C/EBPβ was markedly elevated in tumor-associated Mφ both in vitro and human tumors in situ. The expression of C/EBPβ protein correlated with cytokine production in tumor-activated monocytes. Moreover, we found that C/EBPβ expression was regulated at the post-transcriptional level and correlated with sustained reduction of microRNA-155 （miR-155） in tumor-activated monocytes. Bioinformatic analysis revealed that C/EBPβ is a potential target of miR-155 and luciferase assay confirmed that C/EBPβ translation is suppressed by miR-155 through interaction with the 3＇UTR of C/EBPβ mRNA. Further analysis showed that induction of miR-155 suppressed C/EBPβ protein expression as well as cytokine production in tumor-activated monocytes, an effect which could be mimicked by silencing of C/EBPβ. These results indicate that tumor environment causes a sustained reduction of miR-155 in monocytes/Mφ, which in turn regulates the functional activities of monocytes/Mφ by releasing the translational inhibition of transcription factor C/EBPβ. |
| doi_str_mv | 10.1038/cmi.2009.45 |
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We have recently found that tumors can alter the normal developmental process of Mφ to trigger transient activation of monocytes, but the underlying regulatory mechanisms are incompletely understood. Here, we showed that the protein expression of transcription factor C/EBPβ was markedly elevated in tumor-associated Mφ both in vitro and human tumors in situ. The expression of C/EBPβ protein correlated with cytokine production in tumor-activated monocytes. Moreover, we found that C/EBPβ expression was regulated at the post-transcriptional level and correlated with sustained reduction of microRNA-155 （miR-155） in tumor-activated monocytes. Bioinformatic analysis revealed that C/EBPβ is a potential target of miR-155 and luciferase assay confirmed that C/EBPβ translation is suppressed by miR-155 through interaction with the 3＇UTR of C/EBPβ mRNA. Further analysis showed that induction of miR-155 suppressed C/EBPβ protein expression as well as cytokine production in tumor-activated monocytes, an effect which could be mimicked by silencing of C/EBPβ. These results indicate that tumor environment causes a sustained reduction of miR-155 in monocytes/Mφ, which in turn regulates the functional activities of monocytes/Mφ by releasing the translational inhibition of transcription factor C/EBPβ.</description><identifier>ISSN: 1672-7681</identifier><identifier>EISSN: 2042-0226</identifier><identifier>DOI: 10.1038/cmi.2009.45</identifier><identifier>PMID: 19887047</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>3' Untranslated regions ; Antibodies ; Biomedical and Life Sciences ; Biomedicine ; Cell activation ; Cytokines ; Immunology ; Inflammation ; Macrophages ; Medical Microbiology ; Microbiology ; Microenvironments ; microRNA ; MicroRNAs ; miRNA ; Monocytes ; Phenotypes ; Post-transcription ; Protein expression ; Proteins ; Solid tumors ; Transcription factors ; Tumors ; Vaccine ; 单核细胞 ; 巨噬细胞 ; 微RNA ; 细胞因子 ; 过定位</subject><ispartof>Cellular & molecular immunology, 2009-10, Vol.6 (5), p.343-352</ispartof><rights>The Chinese Society of Immunology 2009</rights><rights>The Chinese Society of Immunology 2009.</rights><rights>Copyright © Wanfang Data Co. 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All Rights Reserved.</rights><rights>Copyright © 2009 The Chinese Society of Immunology 2009 The Chinese Society of Immunology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-8b5ea844a8e88536ae960dc1230fd022b1b0deacd44bc86355a70f5f1ef8256f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/87787X/87787X.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4003217/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4003217/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids></links><search><creatorcontrib>He, Min</creatorcontrib><creatorcontrib>Xu, Zhenqun</creatorcontrib><creatorcontrib>Ding, Tong</creatorcontrib><creatorcontrib>Kuang, Dong-Ming</creatorcontrib><creatorcontrib>Zheng, Limin</creatorcontrib><title>MicroRNA-155 Regulates Inflammatory Cytokine Production in Tumor-associated Macrophages via Targeting C/EBPβ</title><title>Cellular & molecular immunology</title><addtitle>Cell Mol Immunol</addtitle><addtitle>Cellular ＆ Molecular Immunology</addtitle><description>Macrophages （Mφ） are prominent components of solid tumors and exhibit distinct phenotypes in different microenvironments. We have recently found that tumors can alter the normal developmental process of Mφ to trigger transient activation of monocytes, but the underlying regulatory mechanisms are incompletely understood. Here, we showed that the protein expression of transcription factor C/EBPβ was markedly elevated in tumor-associated Mφ both in vitro and human tumors in situ. The expression of C/EBPβ protein correlated with cytokine production in tumor-activated monocytes. Moreover, we found that C/EBPβ expression was regulated at the post-transcriptional level and correlated with sustained reduction of microRNA-155 （miR-155） in tumor-activated monocytes. Bioinformatic analysis revealed that C/EBPβ is a potential target of miR-155 and luciferase assay confirmed that C/EBPβ translation is suppressed by miR-155 through interaction with the 3＇UTR of C/EBPβ mRNA. Further analysis showed that induction of miR-155 suppressed C/EBPβ protein expression as well as cytokine production in tumor-activated monocytes, an effect which could be mimicked by silencing of C/EBPβ. These results indicate that tumor environment causes a sustained reduction of miR-155 in monocytes/Mφ, which in turn regulates the functional activities of monocytes/Mφ by releasing the translational inhibition of transcription factor C/EBPβ.</description><subject>3' Untranslated regions</subject><subject>Antibodies</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell activation</subject><subject>Cytokines</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Macrophages</subject><subject>Medical Microbiology</subject><subject>Microbiology</subject><subject>Microenvironments</subject><subject>microRNA</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Monocytes</subject><subject>Phenotypes</subject><subject>Post-transcription</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Solid tumors</subject><subject>Transcription factors</subject><subject>Tumors</subject><subject>Vaccine</subject><subject>单核细胞</subject><subject>巨噬细胞</subject><subject>微RNA</subject><subject>细胞因子</subject><subject>过定位</subject><issn>1672-7681</issn><issn>2042-0226</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkcFu1DAQhi0EokvhxAtEcAOytR078V4qlVWBSi1U1XK2Jo6ddZvYWzsp7D5WH6TPhFe7alWJ0xz8zTfj-RF6T_CU4EIcqd5OKcazKeMv0IRiRnNMafkSTUhZ0bwqBTlAb2K8xpgLVrHX6IDMhKgwqyaov7Aq-KufJznhPLvS7djBoGN25kwHfQ-DD-tsvh78jXU6uwy-GdVgvcusyxZj70MOMXplU1OTXUByrZbQJsGdhWwBodWDdW02Pzr9evlw_xa9MtBF_W5fD9Hvb6eL-Y_8_Nf3s_nJea4Yp0Muaq5BMAZCC8GLEvSsxI0itMCmSX-rSY0bDaphrFaiLDiHChtuiDaC8tIUh-h4512Nda8bpd0QoJOrYHsIa-nByucvzi5l6-8kw7igpEqCTzvBH3AGXCuv_RhcWllu2n79d7ORentyzDFmCf64nxb87ajj8ETTqkwRsRkhifq8o9KNYgzaPK5DsNwGKVOQcmuVjCf6y46OiXKtDk_O_-Mf9vKld-1t6pA1qBtjOy0LSklJClH8Axv2qz8</recordid><startdate>20091001</startdate><enddate>20091001</enddate><creator>He, Min</creator><creator>Xu, Zhenqun</creator><creator>Ding, Tong</creator><creator>Kuang, Dong-Ming</creator><creator>Zheng, Limin</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><general>Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, China</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W94</scope><scope>WU4</scope><scope>~WA</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope><scope>5PM</scope></search><sort><creationdate>20091001</creationdate><title>MicroRNA-155 Regulates Inflammatory Cytokine Production in Tumor-associated Macrophages via Targeting C/EBPβ</title><author>He, Min ; 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We have recently found that tumors can alter the normal developmental process of Mφ to trigger transient activation of monocytes, but the underlying regulatory mechanisms are incompletely understood. Here, we showed that the protein expression of transcription factor C/EBPβ was markedly elevated in tumor-associated Mφ both in vitro and human tumors in situ. The expression of C/EBPβ protein correlated with cytokine production in tumor-activated monocytes. Moreover, we found that C/EBPβ expression was regulated at the post-transcriptional level and correlated with sustained reduction of microRNA-155 （miR-155） in tumor-activated monocytes. Bioinformatic analysis revealed that C/EBPβ is a potential target of miR-155 and luciferase assay confirmed that C/EBPβ translation is suppressed by miR-155 through interaction with the 3＇UTR of C/EBPβ mRNA. Further analysis showed that induction of miR-155 suppressed C/EBPβ protein expression as well as cytokine production in tumor-activated monocytes, an effect which could be mimicked by silencing of C/EBPβ. These results indicate that tumor environment causes a sustained reduction of miR-155 in monocytes/Mφ, which in turn regulates the functional activities of monocytes/Mφ by releasing the translational inhibition of transcription factor C/EBPβ.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>19887047</pmid><doi>10.1038/cmi.2009.45</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3' Untranslated regions Antibodies Biomedical and Life Sciences Biomedicine Cell activation Cytokines Immunology Inflammation Macrophages Medical Microbiology Microbiology Microenvironments microRNA MicroRNAs miRNA Monocytes Phenotypes Post-transcription Protein expression Proteins Solid tumors Transcription factors Tumors Vaccine 单核细胞 巨噬细胞 微RNA 细胞因子 过定位 |
| title | MicroRNA-155 Regulates Inflammatory Cytokine Production in Tumor-associated Macrophages via Targeting C/EBPβ |
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