microRNA-9 suppresses the proliferation, invasion and metastasis of gastric cancer cells through targeting cyclin D1 and Ets1
Recent evidence shows that altered microRNA-9 (miR-9) expression is implicated in the progression of gastric cancer. However, the exact roles and underlying mechanisms of miR-9 in the proliferation, invasion and metastasis of gastric cancer still remain unknown. In this study, miR-9 was found to be...
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| creator | Zheng, Liduan Qi, Teng Yang, Dehua Qi, Meng Li, Dan Xiang, Xuan Huang, Kai Tong, Qiangsong |
| description | Recent evidence shows that altered microRNA-9 (miR-9) expression is implicated in the progression of gastric cancer. However, the exact roles and underlying mechanisms of miR-9 in the proliferation, invasion and metastasis of gastric cancer still remain unknown. In this study, miR-9 was found to be down-regulated and inversely correlated with the expression of cyclin D1 and v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets1) in gastric cancer tissues and cell lines. Bioinformatics analysis revealed the putative miR-9 binding sites in the 3'-untranslated regions (3'-UTR) of cyclin D1 and Ets1 mRNA. Ectopic expression or knockdown of miR-9 resulted in responsively altered expression of cyclin D1, Ets1 and their downstream targets phosphorylated retinoblastoma and matrix metalloproteinase 9 in cultured gastric cancer cell lines SGC-7901 and AGS. In the luciferase reporter system, miR-9 directly targeted the 3'-UTR of cyclin D1 and Ets1, and these effects were abolished by mutating the miR-9 binding sites. Over-expression of miR-9 suppressed the proliferation, invasion, and metastasis of SGC-7901 and AGS cells in vitro and in vivo. Restoration of miR-9-mediated down-regulation of cyclin D1 and Ets1 by transient transfection, rescued the cancer cells from decrease in proliferation, migration and invasion. Furthermore, anti-miR-9 inhibitor promoted the proliferation, migration and invasion of gastric cancer cells, while knocking down of cyclin D1 or Ets1 partially phenocopied the effects of miR-9 over-expression. These data indicate that miR-9 suppresses the expression of cyclin D1 and Ets1 via the binding sites in their 3'-UTR, thus inhibiting the proliferation, invasion and metastasis of gastric cancer. |
| doi_str_mv | 10.1371/journal.pone.0055719 |
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However, the exact roles and underlying mechanisms of miR-9 in the proliferation, invasion and metastasis of gastric cancer still remain unknown. In this study, miR-9 was found to be down-regulated and inversely correlated with the expression of cyclin D1 and v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets1) in gastric cancer tissues and cell lines. Bioinformatics analysis revealed the putative miR-9 binding sites in the 3'-untranslated regions (3'-UTR) of cyclin D1 and Ets1 mRNA. Ectopic expression or knockdown of miR-9 resulted in responsively altered expression of cyclin D1, Ets1 and their downstream targets phosphorylated retinoblastoma and matrix metalloproteinase 9 in cultured gastric cancer cell lines SGC-7901 and AGS. In the luciferase reporter system, miR-9 directly targeted the 3'-UTR of cyclin D1 and Ets1, and these effects were abolished by mutating the miR-9 binding sites. Over-expression of miR-9 suppressed the proliferation, invasion, and metastasis of SGC-7901 and AGS cells in vitro and in vivo. Restoration of miR-9-mediated down-regulation of cyclin D1 and Ets1 by transient transfection, rescued the cancer cells from decrease in proliferation, migration and invasion. Furthermore, anti-miR-9 inhibitor promoted the proliferation, migration and invasion of gastric cancer cells, while knocking down of cyclin D1 or Ets1 partially phenocopied the effects of miR-9 over-expression. These data indicate that miR-9 suppresses the expression of cyclin D1 and Ets1 via the binding sites in their 3'-UTR, thus inhibiting the proliferation, invasion and metastasis of gastric cancer.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0055719</identifier><identifier>PMID: 23383271</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>3' Untranslated regions ; Analysis ; Angiogenesis ; Apoptosis ; Base Sequence ; Binding sites ; Bioinformatics ; Biology ; Biotechnology ; Cancer ; Cancer cells ; Cancer metastasis ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation ; Cyclin D1 ; Cyclin D1 - genetics ; Development and progression ; Ectopic expression ; Ets-1 protein ; Gastric cancer ; Gene expression ; Gene Expression Regulation, Neoplastic ; Homology ; Humans ; Leukemia ; Luciferase ; Lymphoma ; Mammals ; Matrix metalloproteinase ; Medical prognosis ; Medicine ; Metalloproteinase ; Metastases ; Metastasis ; MicroRNA ; MicroRNAs ; MicroRNAs - chemistry ; MicroRNAs - genetics ; miRNA ; mRNA ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neuroblastoma ; Overexpression ; Pathology ; Proto-Oncogene Protein c-ets-1 - genetics ; Restoration ; Retina ; Retinoblastoma ; Ribonucleic acid ; RNA ; RNA Interference ; RNA Processing, Post-Transcriptional ; Science ; Stomach cancer ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Surgery ; Tissues ; Transfection ; Tumor Burden - genetics ; Tumor cell lines ; Viruses</subject><ispartof>PloS one, 2013-01, Vol.8 (1), p.e55719-e55719</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Zheng 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 Zheng et al 2013 Zheng et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-7bdbc93a4739ba0197ea0699ce021d6868b7d58643b8afdd0035c58b031636ae3</citedby><cites>FETCH-LOGICAL-c758t-7bdbc93a4739ba0197ea0699ce021d6868b7d58643b8afdd0035c58b031636ae3</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/PMC3561302/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561302/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23383271$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, Liduan</creatorcontrib><creatorcontrib>Qi, Teng</creatorcontrib><creatorcontrib>Yang, Dehua</creatorcontrib><creatorcontrib>Qi, Meng</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Xiang, Xuan</creatorcontrib><creatorcontrib>Huang, Kai</creatorcontrib><creatorcontrib>Tong, Qiangsong</creatorcontrib><title>microRNA-9 suppresses the proliferation, invasion and metastasis of gastric cancer cells through targeting cyclin D1 and Ets1</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Recent evidence shows that altered microRNA-9 (miR-9) expression is implicated in the progression of gastric cancer. However, the exact roles and underlying mechanisms of miR-9 in the proliferation, invasion and metastasis of gastric cancer still remain unknown. In this study, miR-9 was found to be down-regulated and inversely correlated with the expression of cyclin D1 and v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets1) in gastric cancer tissues and cell lines. Bioinformatics analysis revealed the putative miR-9 binding sites in the 3'-untranslated regions (3'-UTR) of cyclin D1 and Ets1 mRNA. Ectopic expression or knockdown of miR-9 resulted in responsively altered expression of cyclin D1, Ets1 and their downstream targets phosphorylated retinoblastoma and matrix metalloproteinase 9 in cultured gastric cancer cell lines SGC-7901 and AGS. In the luciferase reporter system, miR-9 directly targeted the 3'-UTR of cyclin D1 and Ets1, and these effects were abolished by mutating the miR-9 binding sites. Over-expression of miR-9 suppressed the proliferation, invasion, and metastasis of SGC-7901 and AGS cells in vitro and in vivo. Restoration of miR-9-mediated down-regulation of cyclin D1 and Ets1 by transient transfection, rescued the cancer cells from decrease in proliferation, migration and invasion. Furthermore, anti-miR-9 inhibitor promoted the proliferation, migration and invasion of gastric cancer cells, while knocking down of cyclin D1 or Ets1 partially phenocopied the effects of miR-9 over-expression. These data indicate that miR-9 suppresses the expression of cyclin D1 and Ets1 via the binding sites in their 3'-UTR, thus inhibiting the proliferation, invasion and metastasis of gastric cancer.</description><subject>3' Untranslated regions</subject><subject>Analysis</subject><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Binding sites</subject><subject>Bioinformatics</subject><subject>Biology</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer metastasis</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation</subject><subject>Cyclin D1</subject><subject>Cyclin D1 - genetics</subject><subject>Development and progression</subject><subject>Ectopic expression</subject><subject>Ets-1 protein</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Homology</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Luciferase</subject><subject>Lymphoma</subject><subject>Mammals</subject><subject>Matrix metalloproteinase</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Metalloproteinase</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - chemistry</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>mRNA</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Metastasis</subject><subject>Neuroblastoma</subject><subject>Overexpression</subject><subject>Pathology</subject><subject>Proto-Oncogene Protein c-ets-1 - genetics</subject><subject>Restoration</subject><subject>Retina</subject><subject>Retinoblastoma</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA Interference</subject><subject>RNA Processing, Post-Transcriptional</subject><subject>Science</subject><subject>Stomach cancer</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Surgery</subject><subject>Tissues</subject><subject>Transfection</subject><subject>Tumor Burden - genetics</subject><subject>Tumor cell lines</subject><subject>Viruses</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>eNqNk11rFDEUhgdRbK3-A9GAIArumo-ZJHMjLLXqQrFQP25DJsnMZpmdjEmm2Av_u5nutOxILySBHJLnvCc5OSfLniO4RISh91s3-E62y951ZglhUTBUPsiOUUnwgmJIHh7YR9mTELYJIpzSx9kRJoQTzNBx9mdnlXeXX1eLEoSh770JwQQQNwb03rW2Nl5G67p3wHZXMiQLyE6DnYkypGkDcDVoku2tAkp2ynigTNuOEt4NzQZE6RsTbdcAda1a24GP6EbiLAb0NHtUyzaYZ9N6kv34dPb99Mvi_OLz-nR1vlCs4HHBKl2pksickbKSEJXMSEjLUhmIkaac8orpgtOcVFzWWkNIClXwChJECZWGnGQv97p964KYMhcEIphDDEvEErHeE9rJrei93Ul_LZy04mbD-UZIH61qjWBlhWquGOE1zmGtK81LrSTiuqIVZHXS-jBFG6qd0cp00ct2Jjo_6exGNO5KkIIiAnESeDMJePdrMCGKnQ1jVmVn3JDujXlOMU6_mdBX_6D3v26iGpkeYLvapbhqFBWrnLESU0Zoopb3UGlok6oklVlt0_7M4e3MITHR_I6NHEIQ62-X_89e_Jyzrw_YjZFt3ATXDmMhhjmY78FUwyF4U98lGUExdsltNsTYJWLqkuT24vCD7pxu24L8Bf15DcU</recordid><startdate>20130131</startdate><enddate>20130131</enddate><creator>Zheng, Liduan</creator><creator>Qi, Teng</creator><creator>Yang, Dehua</creator><creator>Qi, Meng</creator><creator>Li, Dan</creator><creator>Xiang, Xuan</creator><creator>Huang, Kai</creator><creator>Tong, Qiangsong</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>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130131</creationdate><title>microRNA-9 suppresses the proliferation, invasion and metastasis of gastric cancer cells through targeting cyclin D1 and Ets1</title><author>Zheng, Liduan ; Qi, Teng ; Yang, Dehua ; Qi, Meng ; Li, Dan ; Xiang, Xuan ; Huang, Kai ; Tong, Qiangsong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-7bdbc93a4739ba0197ea0699ce021d6868b7d58643b8afdd0035c58b031636ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>3' Untranslated regions</topic><topic>Analysis</topic><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Binding sites</topic><topic>Bioinformatics</topic><topic>Biology</topic><topic>Biotechnology</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cancer metastasis</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - 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Academic</collection><collection>PubMed Central (Full Participant titles)</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>Zheng, Liduan</au><au>Qi, Teng</au><au>Yang, Dehua</au><au>Qi, Meng</au><au>Li, Dan</au><au>Xiang, Xuan</au><au>Huang, Kai</au><au>Tong, Qiangsong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>microRNA-9 suppresses the proliferation, invasion and metastasis of gastric cancer cells through targeting cyclin D1 and Ets1</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-01-31</date><risdate>2013</risdate><volume>8</volume><issue>1</issue><spage>e55719</spage><epage>e55719</epage><pages>e55719-e55719</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Recent evidence shows that altered microRNA-9 (miR-9) expression is implicated in the progression of gastric cancer. However, the exact roles and underlying mechanisms of miR-9 in the proliferation, invasion and metastasis of gastric cancer still remain unknown. In this study, miR-9 was found to be down-regulated and inversely correlated with the expression of cyclin D1 and v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets1) in gastric cancer tissues and cell lines. Bioinformatics analysis revealed the putative miR-9 binding sites in the 3'-untranslated regions (3'-UTR) of cyclin D1 and Ets1 mRNA. Ectopic expression or knockdown of miR-9 resulted in responsively altered expression of cyclin D1, Ets1 and their downstream targets phosphorylated retinoblastoma and matrix metalloproteinase 9 in cultured gastric cancer cell lines SGC-7901 and AGS. In the luciferase reporter system, miR-9 directly targeted the 3'-UTR of cyclin D1 and Ets1, and these effects were abolished by mutating the miR-9 binding sites. Over-expression of miR-9 suppressed the proliferation, invasion, and metastasis of SGC-7901 and AGS cells in vitro and in vivo. Restoration of miR-9-mediated down-regulation of cyclin D1 and Ets1 by transient transfection, rescued the cancer cells from decrease in proliferation, migration and invasion. Furthermore, anti-miR-9 inhibitor promoted the proliferation, migration and invasion of gastric cancer cells, while knocking down of cyclin D1 or Ets1 partially phenocopied the effects of miR-9 over-expression. These data indicate that miR-9 suppresses the expression of cyclin D1 and Ets1 via the binding sites in their 3'-UTR, thus inhibiting the proliferation, invasion and metastasis of gastric cancer.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23383271</pmid><doi>10.1371/journal.pone.0055719</doi><tpages>e55719</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1328020917 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 3' Untranslated regions Analysis Angiogenesis Apoptosis Base Sequence Binding sites Bioinformatics Biology Biotechnology Cancer Cancer cells Cancer metastasis Cell Line, Tumor Cell Movement - genetics Cell Proliferation Cyclin D1 Cyclin D1 - genetics Development and progression Ectopic expression Ets-1 protein Gastric cancer Gene expression Gene Expression Regulation, Neoplastic Homology Humans Leukemia Luciferase Lymphoma Mammals Matrix metalloproteinase Medical prognosis Medicine Metalloproteinase Metastases Metastasis MicroRNA MicroRNAs MicroRNAs - chemistry MicroRNAs - genetics miRNA mRNA Neoplasm Invasiveness Neoplasm Metastasis Neuroblastoma Overexpression Pathology Proto-Oncogene Protein c-ets-1 - genetics Restoration Retina Retinoblastoma Ribonucleic acid RNA RNA Interference RNA Processing, Post-Transcriptional Science Stomach cancer Stomach Neoplasms - genetics Stomach Neoplasms - pathology Surgery Tissues Transfection Tumor Burden - genetics Tumor cell lines Viruses |
| title | microRNA-9 suppresses the proliferation, invasion and metastasis of gastric cancer cells through targeting cyclin D1 and Ets1 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T03%3A04%3A42IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=microRNA-9%20suppresses%20the%20proliferation,%20invasion%20and%20metastasis%20of%20gastric%20cancer%20cells%20through%20targeting%20cyclin%20D1%20and%20Ets1&rft.jtitle=PloS%20one&rft.au=Zheng,%20Liduan&rft.date=2013-01-31&rft.volume=8&rft.issue=1&rft.spage=e55719&rft.epage=e55719&rft.pages=e55719-e55719&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0055719&rft_dat=%3Cgale_plos_%3EA477926736%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1328020917&rft_id=info:pmid/23383271&rft_galeid=A477926736&rft_doaj_id=oai_doaj_org_article_79b1f8c738f240fdbd89dca18db6b07f&rfr_iscdi=true |