MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene
The microRNA miR-138 is dysregulated in several human cancers, but the underlying mechanism remains largely unknown. Here, we report that miR-138 is commonly underexpressed in nasopharyngeal carcinoma (NPC) specimens and NPC cell lines. The ectopic expression of miR-138 dramatically suppressed cell...
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| Veröffentlicht in: | Cell cycle (Georgetown, Tex.) Tex.), 2012-07, Vol.11 (13), p.2495-2506 |
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| creator | Liu, Xia LV, Xiao-Bin Wang, Xiao-Pai Sang, Yi Xu, Shuangbing Hu, Kaishun Wu, Mansi Liang, Yi Liu, Pan Tang, Jianjun Lu, Wen-Hua Feng, Qi-Sheng Chen, Li-Zhen Qian, Chao-Nan Bei, Jin-Xin Kang, Tiebang Zeng, Yi-Xin |
| description | The microRNA miR-138 is dysregulated in several human cancers, but the underlying mechanism remains largely unknown. Here, we report that miR-138 is commonly underexpressed in nasopharyngeal carcinoma (NPC) specimens and NPC cell lines. The ectopic expression of miR-138 dramatically suppressed cell proliferation and colony formation in vitro and inhibited tumorigenesis in vivo. Moreover, we identified the cyclin D1 (CCND1) gene as a novel direct target of miR-138. In consistent with the knocked-down expression of CCND1, overexpression of miR-138 inhibited cell growth and cell cycle progression in NPC cells. Furthermore, CCND1 was widely upregulated in NPC tumors, and its mRNA levels were inversely correlated with miR-138 expression. Taken together, our findings suggest that miR-138 might be a tumor suppressor in NPC, which is exerted partially by inhibiting CCND1 expression. The identification of functional miR-138 in NPC and its direct link to CCND1 might provide good candidates for developing diagnostic markers and therapeutic applications for NPC. |
| doi_str_mv | 10.4161/cc.20898 |
| format | Article |
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Here, we report that miR-138 is commonly underexpressed in nasopharyngeal carcinoma (NPC) specimens and NPC cell lines. The ectopic expression of miR-138 dramatically suppressed cell proliferation and colony formation in vitro and inhibited tumorigenesis in vivo. Moreover, we identified the cyclin D1 (CCND1) gene as a novel direct target of miR-138. In consistent with the knocked-down expression of CCND1, overexpression of miR-138 inhibited cell growth and cell cycle progression in NPC cells. Furthermore, CCND1 was widely upregulated in NPC tumors, and its mRNA levels were inversely correlated with miR-138 expression. Taken together, our findings suggest that miR-138 might be a tumor suppressor in NPC, which is exerted partially by inhibiting CCND1 expression. The identification of functional miR-138 in NPC and its direct link to CCND1 might provide good candidates for developing diagnostic markers and therapeutic applications for NPC.</description><identifier>ISSN: 1538-4101</identifier><identifier>EISSN: 1551-4005</identifier><identifier>DOI: 10.4161/cc.20898</identifier><identifier>PMID: 22739938</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>3' Untranslated Regions ; Animals ; Binding ; Biology ; Bioscience ; Calcium ; Cancer ; Carcinoma ; Cell ; Cell Line, Tumor ; Cell Proliferation ; Cycle ; cyclin D1 (CCND1) ; Cyclin D1 - antagonists & inhibitors ; Cyclin D1 - genetics ; Cyclin D1 - metabolism ; G1 Phase Cell Cycle Checkpoints ; Humans ; Landes ; Mice ; Mice, Nude ; microarray ; microRNA ; MicroRNAs - metabolism ; MicroRNAs - therapeutic use ; miR-138 ; Nasopharyngeal Carcinoma ; nasopharyngeal carcinoma (NPC) ; Nasopharyngeal Neoplasms - drug therapy ; Nasopharyngeal Neoplasms - metabolism ; Nasopharyngeal Neoplasms - pathology ; Organogenesis ; Proteins ; RNA Interference ; RNA, Small Interfering - metabolism ; Transplantation, Heterologous ; tumor suppressor ; tumorigenesis ; Up-Regulation</subject><ispartof>Cell cycle (Georgetown, Tex.), 2012-07, Vol.11 (13), p.2495-2506</ispartof><rights>Copyright © 2012 Landes Bioscience 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-80137b6287c001d8cf41667b3f338acd0975bf4563c5f08605acf6f5e9aa6c843</citedby><cites>FETCH-LOGICAL-c442t-80137b6287c001d8cf41667b3f338acd0975bf4563c5f08605acf6f5e9aa6c843</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22739938$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Xia</creatorcontrib><creatorcontrib>LV, Xiao-Bin</creatorcontrib><creatorcontrib>Wang, Xiao-Pai</creatorcontrib><creatorcontrib>Sang, Yi</creatorcontrib><creatorcontrib>Xu, Shuangbing</creatorcontrib><creatorcontrib>Hu, Kaishun</creatorcontrib><creatorcontrib>Wu, Mansi</creatorcontrib><creatorcontrib>Liang, Yi</creatorcontrib><creatorcontrib>Liu, Pan</creatorcontrib><creatorcontrib>Tang, Jianjun</creatorcontrib><creatorcontrib>Lu, Wen-Hua</creatorcontrib><creatorcontrib>Feng, Qi-Sheng</creatorcontrib><creatorcontrib>Chen, Li-Zhen</creatorcontrib><creatorcontrib>Qian, Chao-Nan</creatorcontrib><creatorcontrib>Bei, Jin-Xin</creatorcontrib><creatorcontrib>Kang, Tiebang</creatorcontrib><creatorcontrib>Zeng, Yi-Xin</creatorcontrib><title>MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene</title><title>Cell cycle (Georgetown, Tex.)</title><addtitle>Cell Cycle</addtitle><description>The microRNA miR-138 is dysregulated in several human cancers, but the underlying mechanism remains largely unknown. Here, we report that miR-138 is commonly underexpressed in nasopharyngeal carcinoma (NPC) specimens and NPC cell lines. The ectopic expression of miR-138 dramatically suppressed cell proliferation and colony formation in vitro and inhibited tumorigenesis in vivo. Moreover, we identified the cyclin D1 (CCND1) gene as a novel direct target of miR-138. In consistent with the knocked-down expression of CCND1, overexpression of miR-138 inhibited cell growth and cell cycle progression in NPC cells. Furthermore, CCND1 was widely upregulated in NPC tumors, and its mRNA levels were inversely correlated with miR-138 expression. Taken together, our findings suggest that miR-138 might be a tumor suppressor in NPC, which is exerted partially by inhibiting CCND1 expression. The identification of functional miR-138 in NPC and its direct link to CCND1 might provide good candidates for developing diagnostic markers and therapeutic applications for NPC.</description><subject>3' Untranslated Regions</subject><subject>Animals</subject><subject>Binding</subject><subject>Biology</subject><subject>Bioscience</subject><subject>Calcium</subject><subject>Cancer</subject><subject>Carcinoma</subject><subject>Cell</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cycle</subject><subject>cyclin D1 (CCND1)</subject><subject>Cyclin D1 - antagonists & inhibitors</subject><subject>Cyclin D1 - genetics</subject><subject>Cyclin D1 - metabolism</subject><subject>G1 Phase Cell Cycle Checkpoints</subject><subject>Humans</subject><subject>Landes</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>microarray</subject><subject>microRNA</subject><subject>MicroRNAs - metabolism</subject><subject>MicroRNAs - therapeutic use</subject><subject>miR-138</subject><subject>Nasopharyngeal Carcinoma</subject><subject>nasopharyngeal carcinoma (NPC)</subject><subject>Nasopharyngeal Neoplasms - drug therapy</subject><subject>Nasopharyngeal Neoplasms - metabolism</subject><subject>Nasopharyngeal Neoplasms - pathology</subject><subject>Organogenesis</subject><subject>Proteins</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Transplantation, Heterologous</subject><subject>tumor suppressor</subject><subject>tumorigenesis</subject><subject>Up-Regulation</subject><issn>1538-4101</issn><issn>1551-4005</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtv1TAQhSNERUtB4hcgL9mk9TNxliiUh1RaqSpryxnbuUaJHexE1f33-HJLu2DBambxnZlzTlW9I_iCk4ZcAlxQLDv5ojojQpCaYyxeHnYma04wOa1e5_wTYyrbjryqTiltWdcxeVaZ7_6uJkyivC1Lsjlbg4LOcdnptA-j1RMCncCHOGs0pviw7pAOBq3bHJMfbbDZZzTs0arTaFcfRrTuLOr7m08ExQDxgLypTpyesn37OM-rH5-v7vuv9fXtl2_9x-saOKdrLTFh7dAUk4AxMRJcCde0A3OMSQ0Gd60YHBcNA-GwbLDQ4BonbKd1A5Kz8-rD8e6S4q_N5lXNPoOdJh1s3LIimLaYk5aKZxRSzDlZp5bk55K5QOrQqQJQfzot6PvHq9swW_ME_i2xAJdHoPwxNg8-ZvA2gH1GMaF9zzHld2oxrijwfxTlu06rh8k-uWBHiQ8uplk_xDQZter9FJNLOoDPiv3j_TebWKTr</recordid><startdate>20120701</startdate><enddate>20120701</enddate><creator>Liu, Xia</creator><creator>LV, Xiao-Bin</creator><creator>Wang, Xiao-Pai</creator><creator>Sang, Yi</creator><creator>Xu, Shuangbing</creator><creator>Hu, Kaishun</creator><creator>Wu, Mansi</creator><creator>Liang, Yi</creator><creator>Liu, Pan</creator><creator>Tang, Jianjun</creator><creator>Lu, Wen-Hua</creator><creator>Feng, Qi-Sheng</creator><creator>Chen, Li-Zhen</creator><creator>Qian, Chao-Nan</creator><creator>Bei, Jin-Xin</creator><creator>Kang, Tiebang</creator><creator>Zeng, Yi-Xin</creator><general>Taylor & Francis</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>7X8</scope></search><sort><creationdate>20120701</creationdate><title>MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene</title><author>Liu, Xia ; LV, Xiao-Bin ; Wang, Xiao-Pai ; Sang, Yi ; Xu, Shuangbing ; Hu, Kaishun ; Wu, Mansi ; Liang, Yi ; Liu, Pan ; Tang, Jianjun ; Lu, Wen-Hua ; Feng, Qi-Sheng ; Chen, Li-Zhen ; Qian, Chao-Nan ; Bei, Jin-Xin ; Kang, Tiebang ; Zeng, Yi-Xin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-80137b6287c001d8cf41667b3f338acd0975bf4563c5f08605acf6f5e9aa6c843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>3' Untranslated Regions</topic><topic>Animals</topic><topic>Binding</topic><topic>Biology</topic><topic>Bioscience</topic><topic>Calcium</topic><topic>Cancer</topic><topic>Carcinoma</topic><topic>Cell</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cycle</topic><topic>cyclin D1 (CCND1)</topic><topic>Cyclin D1 - antagonists & inhibitors</topic><topic>Cyclin D1 - genetics</topic><topic>Cyclin D1 - metabolism</topic><topic>G1 Phase Cell Cycle Checkpoints</topic><topic>Humans</topic><topic>Landes</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>microarray</topic><topic>microRNA</topic><topic>MicroRNAs - metabolism</topic><topic>MicroRNAs - therapeutic use</topic><topic>miR-138</topic><topic>Nasopharyngeal Carcinoma</topic><topic>nasopharyngeal carcinoma (NPC)</topic><topic>Nasopharyngeal Neoplasms - drug therapy</topic><topic>Nasopharyngeal Neoplasms - metabolism</topic><topic>Nasopharyngeal Neoplasms - pathology</topic><topic>Organogenesis</topic><topic>Proteins</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Transplantation, Heterologous</topic><topic>tumor suppressor</topic><topic>tumorigenesis</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Xia</creatorcontrib><creatorcontrib>LV, Xiao-Bin</creatorcontrib><creatorcontrib>Wang, Xiao-Pai</creatorcontrib><creatorcontrib>Sang, Yi</creatorcontrib><creatorcontrib>Xu, Shuangbing</creatorcontrib><creatorcontrib>Hu, Kaishun</creatorcontrib><creatorcontrib>Wu, Mansi</creatorcontrib><creatorcontrib>Liang, Yi</creatorcontrib><creatorcontrib>Liu, Pan</creatorcontrib><creatorcontrib>Tang, Jianjun</creatorcontrib><creatorcontrib>Lu, Wen-Hua</creatorcontrib><creatorcontrib>Feng, Qi-Sheng</creatorcontrib><creatorcontrib>Chen, Li-Zhen</creatorcontrib><creatorcontrib>Qian, Chao-Nan</creatorcontrib><creatorcontrib>Bei, Jin-Xin</creatorcontrib><creatorcontrib>Kang, Tiebang</creatorcontrib><creatorcontrib>Zeng, Yi-Xin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cell cycle (Georgetown, Tex.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Xia</au><au>LV, Xiao-Bin</au><au>Wang, Xiao-Pai</au><au>Sang, Yi</au><au>Xu, Shuangbing</au><au>Hu, Kaishun</au><au>Wu, Mansi</au><au>Liang, Yi</au><au>Liu, Pan</au><au>Tang, Jianjun</au><au>Lu, Wen-Hua</au><au>Feng, Qi-Sheng</au><au>Chen, Li-Zhen</au><au>Qian, Chao-Nan</au><au>Bei, Jin-Xin</au><au>Kang, Tiebang</au><au>Zeng, Yi-Xin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene</atitle><jtitle>Cell cycle (Georgetown, Tex.)</jtitle><addtitle>Cell Cycle</addtitle><date>2012-07-01</date><risdate>2012</risdate><volume>11</volume><issue>13</issue><spage>2495</spage><epage>2506</epage><pages>2495-2506</pages><issn>1538-4101</issn><eissn>1551-4005</eissn><abstract>The microRNA miR-138 is dysregulated in several human cancers, but the underlying mechanism remains largely unknown. Here, we report that miR-138 is commonly underexpressed in nasopharyngeal carcinoma (NPC) specimens and NPC cell lines. The ectopic expression of miR-138 dramatically suppressed cell proliferation and colony formation in vitro and inhibited tumorigenesis in vivo. Moreover, we identified the cyclin D1 (CCND1) gene as a novel direct target of miR-138. In consistent with the knocked-down expression of CCND1, overexpression of miR-138 inhibited cell growth and cell cycle progression in NPC cells. Furthermore, CCND1 was widely upregulated in NPC tumors, and its mRNA levels were inversely correlated with miR-138 expression. Taken together, our findings suggest that miR-138 might be a tumor suppressor in NPC, which is exerted partially by inhibiting CCND1 expression. The identification of functional miR-138 in NPC and its direct link to CCND1 might provide good candidates for developing diagnostic markers and therapeutic applications for NPC.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>22739938</pmid><doi>10.4161/cc.20898</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3' Untranslated Regions Animals Binding Biology Bioscience Calcium Cancer Carcinoma Cell Cell Line, Tumor Cell Proliferation Cycle cyclin D1 (CCND1) Cyclin D1 - antagonists & inhibitors Cyclin D1 - genetics Cyclin D1 - metabolism G1 Phase Cell Cycle Checkpoints Humans Landes Mice Mice, Nude microarray microRNA MicroRNAs - metabolism MicroRNAs - therapeutic use miR-138 Nasopharyngeal Carcinoma nasopharyngeal carcinoma (NPC) Nasopharyngeal Neoplasms - drug therapy Nasopharyngeal Neoplasms - metabolism Nasopharyngeal Neoplasms - pathology Organogenesis Proteins RNA Interference RNA, Small Interfering - metabolism Transplantation, Heterologous tumor suppressor tumorigenesis Up-Regulation |
| title | MiR-138 suppressed nasopharyngeal carcinoma growth and tumorigenesis by targeting the CCND1 oncogene |
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