MicroRNA-452 promotes tumorigenesis in hepatocellular carcinoma by targeting cyclin-dependent kinase inhibitor 1B
Dysregulation of miR-452 has been observed in many tumors, but its biological function in hepatocellular carcinoma (HCC) is still unknown. Our results showed that miR-452 expression is significantly increased in HCC tissues and HCC cell lines. We also found that overexpression of miR-452 dramaticall...
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Veröffentlicht in: | Molecular and cellular biochemistry 2014-04, Vol.389 (1-2), p.187-195 |
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creator | Zheng, Qingliang Sheng, Qing Jiang, Caiying Shu, Jianhong Chen, Jian Nie, Zuoming Lv, Zhengbing Zhang, Yaozhou |
description | Dysregulation of miR-452 has been observed in many tumors, but its biological function in hepatocellular carcinoma (HCC) is still unknown. Our results showed that miR-452 expression is significantly increased in HCC tissues and HCC cell lines. We also found that overexpression of miR-452 dramatically accelerated proliferation, induced cell cycle from G1 to S transition, and blocked apoptosis of HCC cells. Migration and matrigel invasion assays indicated that miR-452 significantly promotes HepG2 and QGY-7703 cells migration and invasion in vitro. Further studies showed that miR-452 directly targets the 3′-untranslated region of cyclin-dependent kinase inhibitor 1B (CDKN1B), ectopic miR-452 expression suppressed CDKN1B expression on mRNA and protein level. Silencing CDKN1B by small interfering RNA resembled the phenotype resulting from ectopic miR-452 expression. This study provides new insights into the potential molecular mechanisms that miRNA-452 contributed to HCC. |
doi_str_mv | 10.1007/s11010-013-1940-z |
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Our results showed that miR-452 expression is significantly increased in HCC tissues and HCC cell lines. We also found that overexpression of miR-452 dramatically accelerated proliferation, induced cell cycle from G1 to S transition, and blocked apoptosis of HCC cells. Migration and matrigel invasion assays indicated that miR-452 significantly promotes HepG2 and QGY-7703 cells migration and invasion in vitro. Further studies showed that miR-452 directly targets the 3′-untranslated region of cyclin-dependent kinase inhibitor 1B (CDKN1B), ectopic miR-452 expression suppressed CDKN1B expression on mRNA and protein level. Silencing CDKN1B by small interfering RNA resembled the phenotype resulting from ectopic miR-452 expression. This study provides new insights into the potential molecular mechanisms that miRNA-452 contributed to HCC.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-013-1940-z</identifier><identifier>PMID: 24381057</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>3' Untranslated Regions - genetics ; Apoptosis ; Apoptosis - genetics ; Biochemistry ; Biomedical and Life Sciences ; Cancer ; Carcinogenesis - genetics ; Carcinoma, Hepatocellular - genetics ; Cardiology ; Cell Line ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation ; Cells ; Cyclin-Dependent Kinase Inhibitor p27 - genetics ; Cyclin-dependent kinases ; Down-Regulation - genetics ; G1 Phase - genetics ; Gene expression ; HEK293 Cells ; Hep G2 Cells ; Hepatoma ; Humans ; Inhibitor drugs ; Life Sciences ; Liver Neoplasms - genetics ; Medical Biochemistry ; MicroRNA ; MicroRNAs - genetics ; Oncology ; RNA, Messenger - genetics ; S Phase - genetics ; Tumorigenesis ; Up-Regulation - genetics</subject><ispartof>Molecular and cellular biochemistry, 2014-04, Vol.389 (1-2), p.187-195</ispartof><rights>Springer Science+Business Media New York 2013</rights><rights>COPYRIGHT 2014 Springer</rights><rights>Springer Science+Business Media New York 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-5288529a8cd7504c72880fe9dc85163ca33122fa63d820c3911184c0ee8b3063</citedby><cites>FETCH-LOGICAL-c538t-5288529a8cd7504c72880fe9dc85163ca33122fa63d820c3911184c0ee8b3063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-013-1940-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-013-1940-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24381057$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, Qingliang</creatorcontrib><creatorcontrib>Sheng, Qing</creatorcontrib><creatorcontrib>Jiang, Caiying</creatorcontrib><creatorcontrib>Shu, Jianhong</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>Nie, Zuoming</creatorcontrib><creatorcontrib>Lv, Zhengbing</creatorcontrib><creatorcontrib>Zhang, Yaozhou</creatorcontrib><title>MicroRNA-452 promotes tumorigenesis in hepatocellular carcinoma by targeting cyclin-dependent kinase inhibitor 1B</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Dysregulation of miR-452 has been observed in many tumors, but its biological function in hepatocellular carcinoma (HCC) is still unknown. Our results showed that miR-452 expression is significantly increased in HCC tissues and HCC cell lines. We also found that overexpression of miR-452 dramatically accelerated proliferation, induced cell cycle from G1 to S transition, and blocked apoptosis of HCC cells. Migration and matrigel invasion assays indicated that miR-452 significantly promotes HepG2 and QGY-7703 cells migration and invasion in vitro. Further studies showed that miR-452 directly targets the 3′-untranslated region of cyclin-dependent kinase inhibitor 1B (CDKN1B), ectopic miR-452 expression suppressed CDKN1B expression on mRNA and protein level. Silencing CDKN1B by small interfering RNA resembled the phenotype resulting from ectopic miR-452 expression. This study provides new insights into the potential molecular mechanisms that miRNA-452 contributed to HCC.</description><subject>3' Untranslated Regions - genetics</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Cardiology</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation</subject><subject>Cells</subject><subject>Cyclin-Dependent Kinase Inhibitor p27 - genetics</subject><subject>Cyclin-dependent kinases</subject><subject>Down-Regulation - genetics</subject><subject>G1 Phase - genetics</subject><subject>Gene expression</subject><subject>HEK293 Cells</subject><subject>Hep G2 Cells</subject><subject>Hepatoma</subject><subject>Humans</subject><subject>Inhibitor drugs</subject><subject>Life Sciences</subject><subject>Liver Neoplasms - genetics</subject><subject>Medical Biochemistry</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>Oncology</subject><subject>RNA, Messenger - genetics</subject><subject>S Phase - genetics</subject><subject>Tumorigenesis</subject><subject>Up-Regulation - genetics</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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><recordid>eNp1kU9v1DAQxS0EotvCB-CCInHh4jJjx-vkuFRQkApIqHfL60y2Lom9tZPD9tPjaMtfgXywPP69pzd6jL1AOEcA_SYjAgIHlBzbGvj9I7ZCpSWvW2wfsxVIAN6g1ifsNOdbKDAgPmUnopYNgtIrdvfJuxS_ft7wWolqn-IYJ8rVNI8x-R0Fyj5XPlQ3tLdTdDQM82BT5WxyPsTRVttDNdm0o8mHXeUObvCBd7Sn0FGYqm8-2EzF4MZv_RRThW-fsSe9HTI9f7jP2PX7d9cXH_jVl8uPF5sr7pRsJq5E0yjR2sZ1WkHtdHlDT23nGoVr6ayUKERv17JrBDjZImJTOyBqthLW8oy9PtqWne5mypMZfV7y20BxzgYVCim0UrKgr_5Cb-OcQglXKFjXoq11_Yva2YGMD32cknWLqdlIDYtTqwp1_g-qnI5G72Kg3pf5HwI8CkoNOSfqzT750aaDQTBLy-bYsiktm6Vlc180Lx8Cz9uRup-KH7UWQByBXL7CjtJvG_3X9TsoQbBG</recordid><startdate>20140401</startdate><enddate>20140401</enddate><creator>Zheng, Qingliang</creator><creator>Sheng, Qing</creator><creator>Jiang, Caiying</creator><creator>Shu, Jianhong</creator><creator>Chen, Jian</creator><creator>Nie, Zuoming</creator><creator>Lv, Zhengbing</creator><creator>Zhang, Yaozhou</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20140401</creationdate><title>MicroRNA-452 promotes tumorigenesis in hepatocellular carcinoma by targeting cyclin-dependent kinase inhibitor 1B</title><author>Zheng, Qingliang ; Sheng, Qing ; Jiang, Caiying ; Shu, Jianhong ; Chen, Jian ; Nie, Zuoming ; Lv, Zhengbing ; Zhang, Yaozhou</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c538t-5288529a8cd7504c72880fe9dc85163ca33122fa63d820c3911184c0ee8b3063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>3' Untranslated Regions - 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genetics</topic><topic>Tumorigenesis</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, Qingliang</creatorcontrib><creatorcontrib>Sheng, Qing</creatorcontrib><creatorcontrib>Jiang, Caiying</creatorcontrib><creatorcontrib>Shu, Jianhong</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>Nie, Zuoming</creatorcontrib><creatorcontrib>Lv, Zhengbing</creatorcontrib><creatorcontrib>Zhang, Yaozhou</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zheng, Qingliang</au><au>Sheng, Qing</au><au>Jiang, Caiying</au><au>Shu, Jianhong</au><au>Chen, Jian</au><au>Nie, Zuoming</au><au>Lv, Zhengbing</au><au>Zhang, Yaozhou</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-452 promotes tumorigenesis in hepatocellular carcinoma by targeting cyclin-dependent kinase inhibitor 1B</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2014-04-01</date><risdate>2014</risdate><volume>389</volume><issue>1-2</issue><spage>187</spage><epage>195</epage><pages>187-195</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Dysregulation of miR-452 has been observed in many tumors, but its biological function in hepatocellular carcinoma (HCC) is still unknown. Our results showed that miR-452 expression is significantly increased in HCC tissues and HCC cell lines. We also found that overexpression of miR-452 dramatically accelerated proliferation, induced cell cycle from G1 to S transition, and blocked apoptosis of HCC cells. Migration and matrigel invasion assays indicated that miR-452 significantly promotes HepG2 and QGY-7703 cells migration and invasion in vitro. Further studies showed that miR-452 directly targets the 3′-untranslated region of cyclin-dependent kinase inhibitor 1B (CDKN1B), ectopic miR-452 expression suppressed CDKN1B expression on mRNA and protein level. Silencing CDKN1B by small interfering RNA resembled the phenotype resulting from ectopic miR-452 expression. This study provides new insights into the potential molecular mechanisms that miRNA-452 contributed to HCC.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24381057</pmid><doi>10.1007/s11010-013-1940-z</doi><tpages>9</tpages></addata></record> |
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subjects | 3' Untranslated Regions - genetics Apoptosis Apoptosis - genetics Biochemistry Biomedical and Life Sciences Cancer Carcinogenesis - genetics Carcinoma, Hepatocellular - genetics Cardiology Cell Line Cell Line, Tumor Cell Movement - genetics Cell Proliferation Cells Cyclin-Dependent Kinase Inhibitor p27 - genetics Cyclin-dependent kinases Down-Regulation - genetics G1 Phase - genetics Gene expression HEK293 Cells Hep G2 Cells Hepatoma Humans Inhibitor drugs Life Sciences Liver Neoplasms - genetics Medical Biochemistry MicroRNA MicroRNAs - genetics Oncology RNA, Messenger - genetics S Phase - genetics Tumorigenesis Up-Regulation - genetics |
title | MicroRNA-452 promotes tumorigenesis in hepatocellular carcinoma by targeting cyclin-dependent kinase inhibitor 1B |
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