miR-1299 suppresses cell proliferation of hepatocellular carcinoma (HCC) by targeting CDK6
Abstract microRNA (miRNA) plays critical role in HCC initiation and development, many miRNAs have been reported to regulate HCC progression. In this study, we studied the role of miR-1299 in cell proliferation of HCC. We found miR-1299 was significantly downregulated in HCC cells and tissues. miR-12...
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| Veröffentlicht in: | Biomedicine & pharmacotherapy 2016-10, Vol.83, p.792-797 |
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| creator | Zhu, Huaqiang Wang, Guangchuan Zhou, Xu Song, Xie Gao, Hengjun Ma, Chaoqun Chang, Hong Li, Hongguang Liu, Fang-feng Lu, Jun Ma, Jinben |
| description | Abstract microRNA (miRNA) plays critical role in HCC initiation and development, many miRNAs have been reported to regulate HCC progression. In this study, we studied the role of miR-1299 in cell proliferation of HCC. We found miR-1299 was significantly downregulated in HCC cells and tissues. miR-1299 overexpression inhibited cell proliferation and arrested cell cycle in G0/G1 phase analyzed by MTT assay, soft agar assay, BrdU cell proliferation assay and cell cycle assay, while miR-1299 knockdown promoted cell proliferation and accelerated G1/S transition. Further analysis suggested the key regulator of G1/S transition, cyclin-dependent kinase 6 (CDK6) was the target of miR-1299, miR-1299 inhibited CDK6 expression and bound to the 3′UTR of CDK6. When double knockdown of miR-1299 and CDK6 promoted cell proliferation copied the phenotype caused by miR-1299 overexpression, suggesting miR-1299 inhibits cell proliferation by targeting CDK6. In summary, our data revealed miR-1299 inhibits cell proliferation, and might be a target for HCC therapy. |
| doi_str_mv | 10.1016/j.biopha.2016.07.037 |
| format | Article |
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In this study, we studied the role of miR-1299 in cell proliferation of HCC. We found miR-1299 was significantly downregulated in HCC cells and tissues. miR-1299 overexpression inhibited cell proliferation and arrested cell cycle in G0/G1 phase analyzed by MTT assay, soft agar assay, BrdU cell proliferation assay and cell cycle assay, while miR-1299 knockdown promoted cell proliferation and accelerated G1/S transition. Further analysis suggested the key regulator of G1/S transition, cyclin-dependent kinase 6 (CDK6) was the target of miR-1299, miR-1299 inhibited CDK6 expression and bound to the 3′UTR of CDK6. When double knockdown of miR-1299 and CDK6 promoted cell proliferation copied the phenotype caused by miR-1299 overexpression, suggesting miR-1299 inhibits cell proliferation by targeting CDK6. In summary, our data revealed miR-1299 inhibits cell proliferation, and might be a target for HCC therapy.</description><identifier>ISSN: 0753-3322</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2016.07.037</identifier><identifier>PMID: 27490780</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Base Sequence ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - pathology ; CDK6 ; Cell Line, Tumor ; Cell Proliferation ; Cyclin-Dependent Kinase 6 - antagonists & inhibitors ; Cyclin-Dependent Kinase 6 - metabolism ; Down-Regulation - genetics ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; HCC ; Humans ; Internal Medicine ; Liver Neoplasms - genetics ; Liver Neoplasms - pathology ; Medical Education ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR-1299</subject><ispartof>Biomedicine & pharmacotherapy, 2016-10, Vol.83, p.792-797</ispartof><rights>2016</rights><rights>Copyright © 2016. Published by Elsevier Masson SAS.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-307731a97fb4a757c16eb92b758ccada24915f99444a983c9c8918e356c7eeb73</citedby><cites>FETCH-LOGICAL-c417t-307731a97fb4a757c16eb92b758ccada24915f99444a983c9c8918e356c7eeb73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.biopha.2016.07.037$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27490780$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Huaqiang</creatorcontrib><creatorcontrib>Wang, Guangchuan</creatorcontrib><creatorcontrib>Zhou, Xu</creatorcontrib><creatorcontrib>Song, Xie</creatorcontrib><creatorcontrib>Gao, Hengjun</creatorcontrib><creatorcontrib>Ma, Chaoqun</creatorcontrib><creatorcontrib>Chang, Hong</creatorcontrib><creatorcontrib>Li, Hongguang</creatorcontrib><creatorcontrib>Liu, Fang-feng</creatorcontrib><creatorcontrib>Lu, Jun</creatorcontrib><creatorcontrib>Ma, Jinben</creatorcontrib><title>miR-1299 suppresses cell proliferation of hepatocellular carcinoma (HCC) by targeting CDK6</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><description>Abstract microRNA (miRNA) plays critical role in HCC initiation and development, many miRNAs have been reported to regulate HCC progression. In this study, we studied the role of miR-1299 in cell proliferation of HCC. We found miR-1299 was significantly downregulated in HCC cells and tissues. miR-1299 overexpression inhibited cell proliferation and arrested cell cycle in G0/G1 phase analyzed by MTT assay, soft agar assay, BrdU cell proliferation assay and cell cycle assay, while miR-1299 knockdown promoted cell proliferation and accelerated G1/S transition. Further analysis suggested the key regulator of G1/S transition, cyclin-dependent kinase 6 (CDK6) was the target of miR-1299, miR-1299 inhibited CDK6 expression and bound to the 3′UTR of CDK6. When double knockdown of miR-1299 and CDK6 promoted cell proliferation copied the phenotype caused by miR-1299 overexpression, suggesting miR-1299 inhibits cell proliferation by targeting CDK6. In summary, our data revealed miR-1299 inhibits cell proliferation, and might be a target for HCC therapy.</description><subject>Base Sequence</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>CDK6</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cyclin-Dependent Kinase 6 - antagonists & inhibitors</subject><subject>Cyclin-Dependent Kinase 6 - metabolism</subject><subject>Down-Regulation - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockdown Techniques</subject><subject>HCC</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - pathology</subject><subject>Medical Education</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR-1299</subject><issn>0753-3322</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1P3DAQhi3UChbKP0CVj3BI6q_Y8QWpCqVURarUj0svluOdgLdJHOyk0v77OlraA5eeRqN5552ZZxC6oKSkhMp3u7L1YXq0JctZSVRJuDpCG6orUkhC1Cu0IariBeeMnaDTlHaEkEry-hidMCU0UTXZoJ-D_1pQpjVOyzRFSAkSdtD3eIqh9x1EO_sw4tDhR5jsHNba0tuInY3Oj2Gw-PKuaa5wu8ezjQ8w-_EBNzef5Rv0urN9gvPneIZ-3H743twV918-fmre3xdOUDUXnCjFqdWqa4VVlXJUQqtZq6raObu1TGhadVoLIayuudOu1rQGXkmnAFrFz9DlwTdv_LRAms3g07qmHSEsydCaSSVYdslScZC6GFKK0Jkp-sHGvaHErFTNzhyompWqIcpkqrnt7fOEpR1g-6_pL8YsuD4IIN_520M0yXkYHWx9BDebbfD_m_DSwPV-9M72v2APaReWOGaGhprEDDHf1s-uj6Uy45Oi5n8AoW2drQ</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Zhu, Huaqiang</creator><creator>Wang, Guangchuan</creator><creator>Zhou, Xu</creator><creator>Song, Xie</creator><creator>Gao, Hengjun</creator><creator>Ma, Chaoqun</creator><creator>Chang, Hong</creator><creator>Li, Hongguang</creator><creator>Liu, Fang-feng</creator><creator>Lu, Jun</creator><creator>Ma, Jinben</creator><general>Elsevier Masson SAS</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>20161001</creationdate><title>miR-1299 suppresses cell proliferation of hepatocellular carcinoma (HCC) by targeting CDK6</title><author>Zhu, Huaqiang ; Wang, Guangchuan ; Zhou, Xu ; Song, Xie ; Gao, Hengjun ; Ma, Chaoqun ; Chang, Hong ; Li, Hongguang ; Liu, Fang-feng ; Lu, Jun ; Ma, Jinben</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-307731a97fb4a757c16eb92b758ccada24915f99444a983c9c8918e356c7eeb73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Base Sequence</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>CDK6</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cyclin-Dependent Kinase 6 - antagonists & inhibitors</topic><topic>Cyclin-Dependent Kinase 6 - metabolism</topic><topic>Down-Regulation - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockdown Techniques</topic><topic>HCC</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - pathology</topic><topic>Medical Education</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR-1299</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Huaqiang</creatorcontrib><creatorcontrib>Wang, Guangchuan</creatorcontrib><creatorcontrib>Zhou, Xu</creatorcontrib><creatorcontrib>Song, Xie</creatorcontrib><creatorcontrib>Gao, Hengjun</creatorcontrib><creatorcontrib>Ma, Chaoqun</creatorcontrib><creatorcontrib>Chang, Hong</creatorcontrib><creatorcontrib>Li, Hongguang</creatorcontrib><creatorcontrib>Liu, Fang-feng</creatorcontrib><creatorcontrib>Lu, Jun</creatorcontrib><creatorcontrib>Ma, Jinben</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>Biomedicine & pharmacotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Huaqiang</au><au>Wang, Guangchuan</au><au>Zhou, Xu</au><au>Song, Xie</au><au>Gao, Hengjun</au><au>Ma, Chaoqun</au><au>Chang, Hong</au><au>Li, Hongguang</au><au>Liu, Fang-feng</au><au>Lu, Jun</au><au>Ma, Jinben</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-1299 suppresses cell proliferation of hepatocellular carcinoma (HCC) by targeting CDK6</atitle><jtitle>Biomedicine & pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>83</volume><spage>792</spage><epage>797</epage><pages>792-797</pages><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract>Abstract microRNA (miRNA) plays critical role in HCC initiation and development, many miRNAs have been reported to regulate HCC progression. In this study, we studied the role of miR-1299 in cell proliferation of HCC. We found miR-1299 was significantly downregulated in HCC cells and tissues. miR-1299 overexpression inhibited cell proliferation and arrested cell cycle in G0/G1 phase analyzed by MTT assay, soft agar assay, BrdU cell proliferation assay and cell cycle assay, while miR-1299 knockdown promoted cell proliferation and accelerated G1/S transition. Further analysis suggested the key regulator of G1/S transition, cyclin-dependent kinase 6 (CDK6) was the target of miR-1299, miR-1299 inhibited CDK6 expression and bound to the 3′UTR of CDK6. When double knockdown of miR-1299 and CDK6 promoted cell proliferation copied the phenotype caused by miR-1299 overexpression, suggesting miR-1299 inhibits cell proliferation by targeting CDK6. In summary, our data revealed miR-1299 inhibits cell proliferation, and might be a target for HCC therapy.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>27490780</pmid><doi>10.1016/j.biopha.2016.07.037</doi><tpages>6</tpages></addata></record> |
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| subjects | Base Sequence Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - pathology CDK6 Cell Line, Tumor Cell Proliferation Cyclin-Dependent Kinase 6 - antagonists & inhibitors Cyclin-Dependent Kinase 6 - metabolism Down-Regulation - genetics Gene Expression Regulation, Neoplastic Gene Knockdown Techniques HCC Humans Internal Medicine Liver Neoplasms - genetics Liver Neoplasms - pathology Medical Education MicroRNAs - genetics MicroRNAs - metabolism miR-1299 |
| title | miR-1299 suppresses cell proliferation of hepatocellular carcinoma (HCC) by targeting CDK6 |
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