MicroRNA-195 inhibits the proliferation of human glioma cells by directly targeting cyclin D1 and cyclin E1
Glioma proliferation is a multistep process during which a sequence of genetic and epigenetic alterations randomly occur to affect the genes controlling cell proliferation, cell death and genetic stability. microRNAs are emerging as important epigenetic modulators of multiple target genes, leading t...
Gespeichert in:
Veröffentlicht in: | PloS one 2013-01, Vol.8 (1), p.e54932 |
---|---|
Hauptverfasser: | , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | |
---|---|
container_issue | 1 |
container_start_page | e54932 |
container_title | PloS one |
container_volume | 8 |
creator | Hui, Wang Yuntao, Lu Lun, Luo WenSheng, Li ChaoFeng, Liang HaiYong, He Yueyang, Ba |
description | Glioma proliferation is a multistep process during which a sequence of genetic and epigenetic alterations randomly occur to affect the genes controlling cell proliferation, cell death and genetic stability. microRNAs are emerging as important epigenetic modulators of multiple target genes, leading to abnormal cellular signaling involving cellular proliferation in cancers.In the present study, we found that expression of miR-195 was markedly downregulated in glioma cell lines and human primary glioma tissues, compared to normal human astrocytes and matched non-tumor associated tissues. Upregulation of miR-195 dramatically reduced the proliferation of glioma cells. Flow cytometry analysis showed that ectopic expression of miR-195 significantly decreased the percentage of S phase cells and increased the percentage of G1/G0 phase cells. Overexpression of miR-195 dramatically reduced the anchorage-independent growth ability of glioma cells. Furthermore, overexpression of miR-195 downregulated the levels of phosphorylated retinoblastoma (pRb) and proliferating cell nuclear antigen (PCNA) in glioma cells. Conversely, inhibition of miR-195 promoted cell proliferation, increased the percentage of S phase cells, reduced the percentage of G1/G0 phase cells, enhanced anchorage-independent growth ability, upregulated the phosphorylation of pRb and PCNA in glioma cells. Moreover, we show that miR-195 inhibited glioma cell proliferation by downregulating expression of cyclin D1 and cyclin E1, via directly targeting the 3'-untranslated regions (3'-UTR) of cyclin D1 and cyclin E1 mRNA. Taken together, our results suggest that miR-195 plays an important role to inhibit the proliferation of glioma cells, and present a novel mechanism for direct miRNA-mediated suppression of cyclin D1 and cyclin E1 in glioma. |
doi_str_mv | 10.1371/journal.pone.0054932 |
format | Article |
fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1327980843</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A477966378</galeid><doaj_id>oai_doaj_org_article_07902bf98a9c4831a1dc3c91ec4909f4</doaj_id><sourcerecordid>A477966378</sourcerecordid><originalsourceid>FETCH-LOGICAL-c692t-cf12dcb711e22bc091916f6fc774d01661e45d4f7551b23b69bc95850ea82ab83</originalsourceid><addsrcrecordid>eNqNkl2LEzEUhgdR3HX1H4gGBMGL1nzMV26Esq5aWF1YP25DJpPMpGaSmmTE_ntTO106oCC5OMnJc96cHN4se4rgEpEKvd640Vtulltn5RLCIqcE38vOUQqLEkNy_2R_lj0KYZMgUpflw-wME1ITCMl59v2jFt7dflotEC2Atr1udAwg9hJsvTNaSc-jdhY4Bfpx4BZ0RruBAyGNCaDZgVZ7KaLZgch9J6O2HRA7YbQFbxHgtj2ertDj7IHiJsgnU7zIvr67-nL5YXF98359ubpeiJLiuBAK4VY0FUIS40ZAiigqValEVeUtRGWJZF60uaqKAjWYNCVtBC3qAkpeY97U5CJ7ftDdGhfYNKfAEMEVrWGdk0SsD0Tr-IZtvR643zHHNfuTcL5j3EctjGSwohA3itacirwmiKNWEEGRFDmFVOVJ68302tgMshXSRs_NTHR-Y3XPOveTkaKoMKVJ4MUk4N2PUYb4j5YnquOpK22VS2Ji0EGwVV5VtCxJtf_68i9UWq0ctEhOUTrlZwWvZgWJifJX7PgYAlt_vv1_9ubbnH15wvaSm9gHZ8a9l8IczA9gsmEIXqq7ySHI9kY_ToPtjc4mo6eyZ6dTvys6Opv8BoNJ93s</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1327980843</pqid></control><display><type>article</type><title>MicroRNA-195 inhibits the proliferation of human glioma cells by directly targeting cyclin D1 and cyclin E1</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Hui, Wang ; Yuntao, Lu ; Lun, Luo ; WenSheng, Li ; ChaoFeng, Liang ; HaiYong, He ; Yueyang, Ba</creator><contributor>Cheng, Jin Q.</contributor><creatorcontrib>Hui, Wang ; Yuntao, Lu ; Lun, Luo ; WenSheng, Li ; ChaoFeng, Liang ; HaiYong, He ; Yueyang, Ba ; Cheng, Jin Q.</creatorcontrib><description>Glioma proliferation is a multistep process during which a sequence of genetic and epigenetic alterations randomly occur to affect the genes controlling cell proliferation, cell death and genetic stability. microRNAs are emerging as important epigenetic modulators of multiple target genes, leading to abnormal cellular signaling involving cellular proliferation in cancers.In the present study, we found that expression of miR-195 was markedly downregulated in glioma cell lines and human primary glioma tissues, compared to normal human astrocytes and matched non-tumor associated tissues. Upregulation of miR-195 dramatically reduced the proliferation of glioma cells. Flow cytometry analysis showed that ectopic expression of miR-195 significantly decreased the percentage of S phase cells and increased the percentage of G1/G0 phase cells. Overexpression of miR-195 dramatically reduced the anchorage-independent growth ability of glioma cells. Furthermore, overexpression of miR-195 downregulated the levels of phosphorylated retinoblastoma (pRb) and proliferating cell nuclear antigen (PCNA) in glioma cells. Conversely, inhibition of miR-195 promoted cell proliferation, increased the percentage of S phase cells, reduced the percentage of G1/G0 phase cells, enhanced anchorage-independent growth ability, upregulated the phosphorylation of pRb and PCNA in glioma cells. Moreover, we show that miR-195 inhibited glioma cell proliferation by downregulating expression of cyclin D1 and cyclin E1, via directly targeting the 3'-untranslated regions (3'-UTR) of cyclin D1 and cyclin E1 mRNA. Taken together, our results suggest that miR-195 plays an important role to inhibit the proliferation of glioma cells, and present a novel mechanism for direct miRNA-mediated suppression of cyclin D1 and cyclin E1 in glioma.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0054932</identifier><identifier>PMID: 23383003</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>3' Untranslated regions ; 3' Untranslated Regions - genetics ; Analysis ; Angiogenesis ; Animals ; Apoptosis ; Astrocytes ; Astrocytes - cytology ; Astrocytes - metabolism ; Base Sequence ; Biology ; Biomarkers, Tumor - metabolism ; Brain cancer ; Brain tumors ; Breast cancer ; Cancer ; Cell cycle ; Cell death ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic ; Cloning ; Control stability ; Cyclin D1 ; Cyclin D1 - genetics ; Cyclin E - genetics ; Cyclin-dependent kinases ; Cytometry ; Down-Regulation - genetics ; Ectopic expression ; Epigenetic inheritance ; Flow cytometry ; Gene expression ; Genes ; Glioma ; Glioma - genetics ; Glioma - pathology ; Glioma cells ; Gliomas ; Hepatology ; Humans ; Kinases ; Liver cancer ; Medical prognosis ; Medicine ; Metastasis ; Mice ; Mice, Inbred BALB C ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Modulators ; mRNA ; Neurosurgery ; Oncogene Proteins - genetics ; Phosphorylation ; Proliferating cell nuclear antigen ; Proliferating Cell Nuclear Antigen - metabolism ; Proteins ; Retina ; Retinoblastoma ; Ribonucleic acid ; RNA ; S phase ; Signaling ; Tissues ; Wang Hui</subject><ispartof>PloS one, 2013-01, Vol.8 (1), p.e54932</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Hui 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 Hui et al 2013 Hui et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-cf12dcb711e22bc091916f6fc774d01661e45d4f7551b23b69bc95850ea82ab83</citedby><cites>FETCH-LOGICAL-c692t-cf12dcb711e22bc091916f6fc774d01661e45d4f7551b23b69bc95850ea82ab83</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/PMC3557299/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3557299/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23383003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Cheng, Jin Q.</contributor><creatorcontrib>Hui, Wang</creatorcontrib><creatorcontrib>Yuntao, Lu</creatorcontrib><creatorcontrib>Lun, Luo</creatorcontrib><creatorcontrib>WenSheng, Li</creatorcontrib><creatorcontrib>ChaoFeng, Liang</creatorcontrib><creatorcontrib>HaiYong, He</creatorcontrib><creatorcontrib>Yueyang, Ba</creatorcontrib><title>MicroRNA-195 inhibits the proliferation of human glioma cells by directly targeting cyclin D1 and cyclin E1</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Glioma proliferation is a multistep process during which a sequence of genetic and epigenetic alterations randomly occur to affect the genes controlling cell proliferation, cell death and genetic stability. microRNAs are emerging as important epigenetic modulators of multiple target genes, leading to abnormal cellular signaling involving cellular proliferation in cancers.In the present study, we found that expression of miR-195 was markedly downregulated in glioma cell lines and human primary glioma tissues, compared to normal human astrocytes and matched non-tumor associated tissues. Upregulation of miR-195 dramatically reduced the proliferation of glioma cells. Flow cytometry analysis showed that ectopic expression of miR-195 significantly decreased the percentage of S phase cells and increased the percentage of G1/G0 phase cells. Overexpression of miR-195 dramatically reduced the anchorage-independent growth ability of glioma cells. Furthermore, overexpression of miR-195 downregulated the levels of phosphorylated retinoblastoma (pRb) and proliferating cell nuclear antigen (PCNA) in glioma cells. Conversely, inhibition of miR-195 promoted cell proliferation, increased the percentage of S phase cells, reduced the percentage of G1/G0 phase cells, enhanced anchorage-independent growth ability, upregulated the phosphorylation of pRb and PCNA in glioma cells. Moreover, we show that miR-195 inhibited glioma cell proliferation by downregulating expression of cyclin D1 and cyclin E1, via directly targeting the 3'-untranslated regions (3'-UTR) of cyclin D1 and cyclin E1 mRNA. Taken together, our results suggest that miR-195 plays an important role to inhibit the proliferation of glioma cells, and present a novel mechanism for direct miRNA-mediated suppression of cyclin D1 and cyclin E1 in glioma.</description><subject>3' Untranslated regions</subject><subject>3' Untranslated Regions - genetics</subject><subject>Analysis</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Astrocytes</subject><subject>Astrocytes - cytology</subject><subject>Astrocytes - metabolism</subject><subject>Base Sequence</subject><subject>Biology</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic</subject><subject>Cloning</subject><subject>Control stability</subject><subject>Cyclin D1</subject><subject>Cyclin D1 - genetics</subject><subject>Cyclin E - genetics</subject><subject>Cyclin-dependent kinases</subject><subject>Cytometry</subject><subject>Down-Regulation - genetics</subject><subject>Ectopic expression</subject><subject>Epigenetic inheritance</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>Gliomas</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Modulators</subject><subject>mRNA</subject><subject>Neurosurgery</subject><subject>Oncogene Proteins - genetics</subject><subject>Phosphorylation</subject><subject>Proliferating cell nuclear antigen</subject><subject>Proliferating Cell Nuclear Antigen - metabolism</subject><subject>Proteins</subject><subject>Retina</subject><subject>Retinoblastoma</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>S phase</subject><subject>Signaling</subject><subject>Tissues</subject><subject>Wang Hui</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>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2LEzEUhgdR3HX1H4gGBMGL1nzMV26Esq5aWF1YP25DJpPMpGaSmmTE_ntTO106oCC5OMnJc96cHN4se4rgEpEKvd640Vtulltn5RLCIqcE38vOUQqLEkNy_2R_lj0KYZMgUpflw-wME1ITCMl59v2jFt7dflotEC2Atr1udAwg9hJsvTNaSc-jdhY4Bfpx4BZ0RruBAyGNCaDZgVZ7KaLZgch9J6O2HRA7YbQFbxHgtj2ertDj7IHiJsgnU7zIvr67-nL5YXF98359ubpeiJLiuBAK4VY0FUIS40ZAiigqValEVeUtRGWJZF60uaqKAjWYNCVtBC3qAkpeY97U5CJ7ftDdGhfYNKfAEMEVrWGdk0SsD0Tr-IZtvR643zHHNfuTcL5j3EctjGSwohA3itacirwmiKNWEEGRFDmFVOVJ68302tgMshXSRs_NTHR-Y3XPOveTkaKoMKVJ4MUk4N2PUYb4j5YnquOpK22VS2Ji0EGwVV5VtCxJtf_68i9UWq0ctEhOUTrlZwWvZgWJifJX7PgYAlt_vv1_9ubbnH15wvaSm9gHZ8a9l8IczA9gsmEIXqq7ySHI9kY_ToPtjc4mo6eyZ6dTvys6Opv8BoNJ93s</recordid><startdate>20130128</startdate><enddate>20130128</enddate><creator>Hui, Wang</creator><creator>Yuntao, Lu</creator><creator>Lun, Luo</creator><creator>WenSheng, Li</creator><creator>ChaoFeng, Liang</creator><creator>HaiYong, He</creator><creator>Yueyang, Ba</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>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130128</creationdate><title>MicroRNA-195 inhibits the proliferation of human glioma cells by directly targeting cyclin D1 and cyclin E1</title><author>Hui, Wang ; Yuntao, Lu ; Lun, Luo ; WenSheng, Li ; ChaoFeng, Liang ; HaiYong, He ; Yueyang, Ba</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-cf12dcb711e22bc091916f6fc774d01661e45d4f7551b23b69bc95850ea82ab83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>3' Untranslated regions</topic><topic>3' Untranslated Regions - genetics</topic><topic>Analysis</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Astrocytes</topic><topic>Astrocytes - cytology</topic><topic>Astrocytes - metabolism</topic><topic>Base Sequence</topic><topic>Biology</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Brain cancer</topic><topic>Brain tumors</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell Transformation, Neoplastic</topic><topic>Cloning</topic><topic>Control stability</topic><topic>Cyclin D1</topic><topic>Cyclin D1 - genetics</topic><topic>Cyclin E - genetics</topic><topic>Cyclin-dependent kinases</topic><topic>Cytometry</topic><topic>Down-Regulation - genetics</topic><topic>Ectopic expression</topic><topic>Epigenetic inheritance</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Glioma</topic><topic>Glioma - genetics</topic><topic>Glioma - pathology</topic><topic>Glioma cells</topic><topic>Gliomas</topic><topic>Hepatology</topic><topic>Humans</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Modulators</topic><topic>mRNA</topic><topic>Neurosurgery</topic><topic>Oncogene Proteins - genetics</topic><topic>Phosphorylation</topic><topic>Proliferating cell nuclear antigen</topic><topic>Proliferating Cell Nuclear Antigen - metabolism</topic><topic>Proteins</topic><topic>Retina</topic><topic>Retinoblastoma</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>S phase</topic><topic>Signaling</topic><topic>Tissues</topic><topic>Wang Hui</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hui, Wang</creatorcontrib><creatorcontrib>Yuntao, Lu</creatorcontrib><creatorcontrib>Lun, Luo</creatorcontrib><creatorcontrib>WenSheng, Li</creatorcontrib><creatorcontrib>ChaoFeng, Liang</creatorcontrib><creatorcontrib>HaiYong, He</creatorcontrib><creatorcontrib>Yueyang, Ba</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</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>Hui, Wang</au><au>Yuntao, Lu</au><au>Lun, Luo</au><au>WenSheng, Li</au><au>ChaoFeng, Liang</au><au>HaiYong, He</au><au>Yueyang, Ba</au><au>Cheng, Jin Q.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-195 inhibits the proliferation of human glioma cells by directly targeting cyclin D1 and cyclin E1</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-01-28</date><risdate>2013</risdate><volume>8</volume><issue>1</issue><spage>e54932</spage><pages>e54932-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Glioma proliferation is a multistep process during which a sequence of genetic and epigenetic alterations randomly occur to affect the genes controlling cell proliferation, cell death and genetic stability. microRNAs are emerging as important epigenetic modulators of multiple target genes, leading to abnormal cellular signaling involving cellular proliferation in cancers.In the present study, we found that expression of miR-195 was markedly downregulated in glioma cell lines and human primary glioma tissues, compared to normal human astrocytes and matched non-tumor associated tissues. Upregulation of miR-195 dramatically reduced the proliferation of glioma cells. Flow cytometry analysis showed that ectopic expression of miR-195 significantly decreased the percentage of S phase cells and increased the percentage of G1/G0 phase cells. Overexpression of miR-195 dramatically reduced the anchorage-independent growth ability of glioma cells. Furthermore, overexpression of miR-195 downregulated the levels of phosphorylated retinoblastoma (pRb) and proliferating cell nuclear antigen (PCNA) in glioma cells. Conversely, inhibition of miR-195 promoted cell proliferation, increased the percentage of S phase cells, reduced the percentage of G1/G0 phase cells, enhanced anchorage-independent growth ability, upregulated the phosphorylation of pRb and PCNA in glioma cells. Moreover, we show that miR-195 inhibited glioma cell proliferation by downregulating expression of cyclin D1 and cyclin E1, via directly targeting the 3'-untranslated regions (3'-UTR) of cyclin D1 and cyclin E1 mRNA. Taken together, our results suggest that miR-195 plays an important role to inhibit the proliferation of glioma cells, and present a novel mechanism for direct miRNA-mediated suppression of cyclin D1 and cyclin E1 in glioma.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23383003</pmid><doi>10.1371/journal.pone.0054932</doi><tpages>e54932</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2013-01, Vol.8 (1), p.e54932 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_1327980843 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | 3' Untranslated regions 3' Untranslated Regions - genetics Analysis Angiogenesis Animals Apoptosis Astrocytes Astrocytes - cytology Astrocytes - metabolism Base Sequence Biology Biomarkers, Tumor - metabolism Brain cancer Brain tumors Breast cancer Cancer Cell cycle Cell death Cell growth Cell Line, Tumor Cell Proliferation Cell Transformation, Neoplastic Cloning Control stability Cyclin D1 Cyclin D1 - genetics Cyclin E - genetics Cyclin-dependent kinases Cytometry Down-Regulation - genetics Ectopic expression Epigenetic inheritance Flow cytometry Gene expression Genes Glioma Glioma - genetics Glioma - pathology Glioma cells Gliomas Hepatology Humans Kinases Liver cancer Medical prognosis Medicine Metastasis Mice Mice, Inbred BALB C MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Modulators mRNA Neurosurgery Oncogene Proteins - genetics Phosphorylation Proliferating cell nuclear antigen Proliferating Cell Nuclear Antigen - metabolism Proteins Retina Retinoblastoma Ribonucleic acid RNA S phase Signaling Tissues Wang Hui |
title | MicroRNA-195 inhibits the proliferation of human glioma cells by directly targeting cyclin D1 and cyclin E1 |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-19T13%3A52%3A12IST&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-195%20inhibits%20the%20proliferation%20of%20human%20glioma%20cells%20by%20directly%20targeting%20cyclin%20D1%20and%20cyclin%20E1&rft.jtitle=PloS%20one&rft.au=Hui,%20Wang&rft.date=2013-01-28&rft.volume=8&rft.issue=1&rft.spage=e54932&rft.pages=e54932-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0054932&rft_dat=%3Cgale_plos_%3EA477966378%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=1327980843&rft_id=info:pmid/23383003&rft_galeid=A477966378&rft_doaj_id=oai_doaj_org_article_07902bf98a9c4831a1dc3c91ec4909f4&rfr_iscdi=true |