Roles and mechanism of miR-199a and miR-125b in tumor angiogenesis
MicroRNAs (miRNAs) have been shown to be involved in different aspects of cancer biology including tumor angiogenesis. In this study, we identified that two miRNAs, miR-199a and miR-125b were downregulated in ovarian cancer tissues and cell lines. Overexpression of miR-199a and miR-125b inhibited tu...
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| creator | He, Jun Jing, Yi Li, Wei Qian, Xu Xu, Qing Li, Feng-Shan Liu, Ling-Zhi Jiang, Bing-Hua Jiang, Yue |
| description | MicroRNAs (miRNAs) have been shown to be involved in different aspects of cancer biology including tumor angiogenesis. In this study, we identified that two miRNAs, miR-199a and miR-125b were downregulated in ovarian cancer tissues and cell lines. Overexpression of miR-199a and miR-125b inhibited tumor-induced angiogenesis associated with the decrease of HIF-1α and VEGF expression in ovarian cancer cells. Moreover, the levels of miR-199a and miR-125b were negatively correlated with VEGF mRNA levels in ovarian tissues. We further showed that direct targets of miR-199a and miR-125b HER2 and HER3 were functionally relevant. Forced expression of HER2 and HER3 rescued miR-199a- and miR-125b-inhibiting angiogenesis responses and Akt/p70S6K1/HIF-1α pathway. This study provides a rationale for new therapeutic approach to suppress tumor angiogenesis using miR-199a, miR-125b, or their mimics for ovarian cancer treatment in the future. |
| doi_str_mv | 10.1371/journal.pone.0056647 |
| format | Article |
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In this study, we identified that two miRNAs, miR-199a and miR-125b were downregulated in ovarian cancer tissues and cell lines. Overexpression of miR-199a and miR-125b inhibited tumor-induced angiogenesis associated with the decrease of HIF-1α and VEGF expression in ovarian cancer cells. Moreover, the levels of miR-199a and miR-125b were negatively correlated with VEGF mRNA levels in ovarian tissues. We further showed that direct targets of miR-199a and miR-125b HER2 and HER3 were functionally relevant. Forced expression of HER2 and HER3 rescued miR-199a- and miR-125b-inhibiting angiogenesis responses and Akt/p70S6K1/HIF-1α pathway. This study provides a rationale for new therapeutic approach to suppress tumor angiogenesis using miR-199a, miR-125b, or their mimics for ovarian cancer treatment in the future.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0056647</identifier><identifier>PMID: 23437196</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>AKT protein ; Angiogenesis ; Biology ; Cancer ; Cancer research ; Cancer treatment ; Cell Movement ; Cell Proliferation ; Down-Regulation ; ErbB-2 protein ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit - genetics ; Kinases ; Medicine ; MicroRNA ; MicroRNAs - genetics ; miRNA ; mRNA ; Neovascularization, Pathologic - genetics ; Ovarian cancer ; Ovarian carcinoma ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - pathology ; Receptor, ErbB-2 - genetics ; Receptor, ErbB-3 - genetics ; Tissues ; Tumor cell lines ; Tumors ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics ; Womens health</subject><ispartof>PloS one, 2013-02, Vol.8 (2), p.e56647-e56647</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 He 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>2013 He et al 2013 He et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-339eebc26469c7a78e70dc174d90f13bda600b3354d073f1322bd7c2bec09cfa3</citedby><cites>FETCH-LOGICAL-c758t-339eebc26469c7a78e70dc174d90f13bda600b3354d073f1322bd7c2bec09cfa3</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/PMC3577861/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3577861/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23437196$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Jun</creatorcontrib><creatorcontrib>Jing, Yi</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Qian, Xu</creatorcontrib><creatorcontrib>Xu, Qing</creatorcontrib><creatorcontrib>Li, Feng-Shan</creatorcontrib><creatorcontrib>Liu, Ling-Zhi</creatorcontrib><creatorcontrib>Jiang, Bing-Hua</creatorcontrib><creatorcontrib>Jiang, Yue</creatorcontrib><title>Roles and mechanism of miR-199a and miR-125b in tumor angiogenesis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>MicroRNAs (miRNAs) have been shown to be involved in different aspects of cancer biology including tumor angiogenesis. In this study, we identified that two miRNAs, miR-199a and miR-125b were downregulated in ovarian cancer tissues and cell lines. Overexpression of miR-199a and miR-125b inhibited tumor-induced angiogenesis associated with the decrease of HIF-1α and VEGF expression in ovarian cancer cells. Moreover, the levels of miR-199a and miR-125b were negatively correlated with VEGF mRNA levels in ovarian tissues. We further showed that direct targets of miR-199a and miR-125b HER2 and HER3 were functionally relevant. Forced expression of HER2 and HER3 rescued miR-199a- and miR-125b-inhibiting angiogenesis responses and Akt/p70S6K1/HIF-1α pathway. This study provides a rationale for new therapeutic approach to suppress tumor angiogenesis using miR-199a, miR-125b, or their mimics for ovarian cancer treatment in the future.</description><subject>AKT protein</subject><subject>Angiogenesis</subject><subject>Biology</subject><subject>Cancer</subject><subject>Cancer research</subject><subject>Cancer treatment</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Down-Regulation</subject><subject>ErbB-2 protein</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</subject><subject>Kinases</subject><subject>Medicine</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>mRNA</subject><subject>Neovascularization, Pathologic - genetics</subject><subject>Ovarian cancer</subject><subject>Ovarian carcinoma</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Receptor, ErbB-3 - genetics</subject><subject>Tissues</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Womens health</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7jr6D0QLguhFx3y0SXsjrIsfAwsL48dtSJPTToY2mU1a0X9v6nSXqeyF7UXTk-e8yZu8SfIcozWmHL_bu9Fb2a0PzsIaoYKxnD9IznFFScYIog9PxmfJkxD2EaIlY4-TM0LzKFGx8-TD1nUQUml12oPaSWtCn7om7c02w1UljzPTDynq1Nh0GHvnY7U1rgULwYSnyaNGdgGezd9V8v3Tx2-XX7Kr68-by4urTPGiHDJKK4BaEZazSnHJS-BIK8xzXaEG01pLhlBNaZFrxGmsEFJrrkgNClWqkXSVvDzqHjoXxGw_CEwpKkuKo6VVsjkS2sm9OHjTS_9bOGnE34LzrZB-MKoDoYnERYMZw4rkFddlzjXEp0GF4oSWUev9vNpY96AV2MHLbiG6nLFmJ1r3U9CC85LhKPBmFvDuZoQwiN4EBV0nLbhx2jcmrOAFmtBX_6D3u5upVkYDxjYurqsmUXGR85KgPNqJ1PoeKr4aeqNiVhoT64uGt4uGyAzwa2jlGILYfN3-P3v9Y8m-PmF3ILthF1w3DsbZsATzI6i8C8FDc3fIGIkp6renIaaoiznqse3F6QXdNd1mm_4BeDP18Q</recordid><startdate>20130220</startdate><enddate>20130220</enddate><creator>He, Jun</creator><creator>Jing, Yi</creator><creator>Li, Wei</creator><creator>Qian, Xu</creator><creator>Xu, Qing</creator><creator>Li, Feng-Shan</creator><creator>Liu, Ling-Zhi</creator><creator>Jiang, Bing-Hua</creator><creator>Jiang, Yue</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>AEUYN</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>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130220</creationdate><title>Roles and mechanism of miR-199a and miR-125b in tumor angiogenesis</title><author>He, Jun ; Jing, Yi ; Li, Wei ; Qian, Xu ; Xu, Qing ; Li, Feng-Shan ; Liu, Ling-Zhi ; Jiang, Bing-Hua ; Jiang, Yue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-339eebc26469c7a78e70dc174d90f13bda600b3354d073f1322bd7c2bec09cfa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>AKT protein</topic><topic>Angiogenesis</topic><topic>Biology</topic><topic>Cancer</topic><topic>Cancer research</topic><topic>Cancer treatment</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Down-Regulation</topic><topic>ErbB-2 protein</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - 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In this study, we identified that two miRNAs, miR-199a and miR-125b were downregulated in ovarian cancer tissues and cell lines. Overexpression of miR-199a and miR-125b inhibited tumor-induced angiogenesis associated with the decrease of HIF-1α and VEGF expression in ovarian cancer cells. Moreover, the levels of miR-199a and miR-125b were negatively correlated with VEGF mRNA levels in ovarian tissues. We further showed that direct targets of miR-199a and miR-125b HER2 and HER3 were functionally relevant. Forced expression of HER2 and HER3 rescued miR-199a- and miR-125b-inhibiting angiogenesis responses and Akt/p70S6K1/HIF-1α pathway. This study provides a rationale for new therapeutic approach to suppress tumor angiogenesis using miR-199a, miR-125b, or their mimics for ovarian cancer treatment in the future.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23437196</pmid><doi>10.1371/journal.pone.0056647</doi><tpages>e56647</tpages><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | AKT protein Angiogenesis Biology Cancer Cancer research Cancer treatment Cell Movement Cell Proliferation Down-Regulation ErbB-2 protein Female Gene Expression Regulation, Neoplastic Humans Hypoxia-Inducible Factor 1, alpha Subunit - genetics Kinases Medicine MicroRNA MicroRNAs - genetics miRNA mRNA Neovascularization, Pathologic - genetics Ovarian cancer Ovarian carcinoma Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Receptor, ErbB-2 - genetics Receptor, ErbB-3 - genetics Tissues Tumor cell lines Tumors Vascular endothelial growth factor Vascular Endothelial Growth Factor A - genetics Womens health |
| title | Roles and mechanism of miR-199a and miR-125b in tumor angiogenesis |
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