miR-25 targets the modulator of apoptosis 1 gene in lung cancer
To determine the role of miR-25 in non-small cell lung cancer (NSCLC), we first detected miR-25 expression in clinical specimens and lung cancer cell lines by quantitative real-time polymerase chain reaction. The levels of miR-25 were elevated in the plasma of NSCLC patients and NSCLC cell lines. Tr...
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| Veröffentlicht in: | Carcinogenesis (New York) 2015-08, Vol.36 (8), p.925-935 |
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| container_title | Carcinogenesis (New York) |
| container_volume | 36 |
| creator | Wu, Tangwei Chen, Weiqun Kong, Deyong Li, Xiaoyi Lu, Hongda Liu, Shuiyi Wang, Jing Du, Lili Kong, Qingzhi Huang, Xiaodong Lu, Zhongxin |
| description | To determine the role of miR-25 in non-small cell lung cancer (NSCLC), we first detected miR-25 expression in clinical specimens and lung cancer cell lines by quantitative real-time polymerase chain reaction. The levels of miR-25 were elevated in the plasma of NSCLC patients and NSCLC cell lines. Transfection of A549 and 95-D cells with a miR-25 inhibitor resulted in reduced cell proliferation and enhanced apoptosis. Moreover, the modulator of apoptosis 1 (MOAP1) gene was identified as a novel target of miR-25. The ability of miR-25 to promote cell proliferation and block apoptosis is attributable to its effect on MOAP1 suppression. In addition, miR-25 antagomir significantly inhibited lung cancer growth via upregulation of MOAP1 in a mouse xenograft model. Collectively, these data demonstrate that miR-25 is an important biomarker for lung cancer, and miR-25 promotes cell proliferation and inhibits apoptosis in NSCLC cells by negatively regulating MOAP1 expression. |
| doi_str_mv | 10.1093/carcin/bgv068 |
| format | Article |
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The levels of miR-25 were elevated in the plasma of NSCLC patients and NSCLC cell lines. Transfection of A549 and 95-D cells with a miR-25 inhibitor resulted in reduced cell proliferation and enhanced apoptosis. Moreover, the modulator of apoptosis 1 (MOAP1) gene was identified as a novel target of miR-25. The ability of miR-25 to promote cell proliferation and block apoptosis is attributable to its effect on MOAP1 suppression. In addition, miR-25 antagomir significantly inhibited lung cancer growth via upregulation of MOAP1 in a mouse xenograft model. Collectively, these data demonstrate that miR-25 is an important biomarker for lung cancer, and miR-25 promotes cell proliferation and inhibits apoptosis in NSCLC cells by negatively regulating MOAP1 expression.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/bgv068</identifier><identifier>PMID: 25998847</identifier><language>eng</language><publisher>England</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Aged ; Animals ; Apoptosis - genetics ; Apoptosis Regulatory Proteins - genetics ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - pathology ; Case-Control Studies ; Cell Line, Tumor ; Cell Proliferation - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Male ; Mice, Inbred BALB C ; MicroRNAs - blood ; MicroRNAs - genetics ; Middle Aged ; Xenograft Model Antitumor Assays</subject><ispartof>Carcinogenesis (New York), 2015-08, Vol.36 (8), p.925-935</ispartof><rights>The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-d6eb617ca5147c4552bb3f0ce0da824904172eaed9a270a31dee94c1bf935dda3</citedby><cites>FETCH-LOGICAL-c392t-d6eb617ca5147c4552bb3f0ce0da824904172eaed9a270a31dee94c1bf935dda3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25998847$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Tangwei</creatorcontrib><creatorcontrib>Chen, Weiqun</creatorcontrib><creatorcontrib>Kong, Deyong</creatorcontrib><creatorcontrib>Li, Xiaoyi</creatorcontrib><creatorcontrib>Lu, Hongda</creatorcontrib><creatorcontrib>Liu, Shuiyi</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Du, Lili</creatorcontrib><creatorcontrib>Kong, Qingzhi</creatorcontrib><creatorcontrib>Huang, Xiaodong</creatorcontrib><creatorcontrib>Lu, Zhongxin</creatorcontrib><title>miR-25 targets the modulator of apoptosis 1 gene in lung cancer</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>To determine the role of miR-25 in non-small cell lung cancer (NSCLC), we first detected miR-25 expression in clinical specimens and lung cancer cell lines by quantitative real-time polymerase chain reaction. The levels of miR-25 were elevated in the plasma of NSCLC patients and NSCLC cell lines. Transfection of A549 and 95-D cells with a miR-25 inhibitor resulted in reduced cell proliferation and enhanced apoptosis. Moreover, the modulator of apoptosis 1 (MOAP1) gene was identified as a novel target of miR-25. The ability of miR-25 to promote cell proliferation and block apoptosis is attributable to its effect on MOAP1 suppression. In addition, miR-25 antagomir significantly inhibited lung cancer growth via upregulation of MOAP1 in a mouse xenograft model. Collectively, these data demonstrate that miR-25 is an important biomarker for lung cancer, and miR-25 promotes cell proliferation and inhibits apoptosis in NSCLC cells by negatively regulating MOAP1 expression.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Aged</subject><subject>Animals</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Case-Control Studies</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Mice, Inbred BALB C</subject><subject>MicroRNAs - blood</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo90EtLxDAYheEgijOOLt1Klm7q5MulbVYiw3iBAUF0XdLka620TU1awX_vSEdXZ_NwFi8hl8BugGmxtibYpl-X9RdL8yOyBJmyhEPOjsmSgRSJEEIuyFmMH4xBKpQ-JQuutM5zmS3Jbde8JFzR0YQax0jHd6Sdd1NrRh-or6gZ_DD62EQKtMYeadPTduprak1vMZyTk8q0ES8OuyJv99vXzWOye3542tztEis0HxOXYplCZo0CmVmpFC9LUTGLzJmcS80kZBwNOm14xowAh6ilhbLSQjlnxIpcz79D8J8TxrHommixbU2PfooFZJBJnbJc7WkyUxt8jAGrYghNZ8J3Aaz4bVbMzYq52d5fHa6nskP3r_8iiR_E02jj</recordid><startdate>20150801</startdate><enddate>20150801</enddate><creator>Wu, Tangwei</creator><creator>Chen, Weiqun</creator><creator>Kong, Deyong</creator><creator>Li, Xiaoyi</creator><creator>Lu, Hongda</creator><creator>Liu, Shuiyi</creator><creator>Wang, Jing</creator><creator>Du, Lili</creator><creator>Kong, Qingzhi</creator><creator>Huang, Xiaodong</creator><creator>Lu, Zhongxin</creator><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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20150801</creationdate><title>miR-25 targets the modulator of apoptosis 1 gene in lung cancer</title><author>Wu, Tangwei ; Chen, Weiqun ; Kong, Deyong ; Li, Xiaoyi ; Lu, Hongda ; Liu, Shuiyi ; Wang, Jing ; Du, Lili ; Kong, Qingzhi ; Huang, Xiaodong ; Lu, Zhongxin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-d6eb617ca5147c4552bb3f0ce0da824904172eaed9a270a31dee94c1bf935dda3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Aged</topic><topic>Animals</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Case-Control Studies</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Mice, Inbred BALB C</topic><topic>MicroRNAs - blood</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Tangwei</creatorcontrib><creatorcontrib>Chen, Weiqun</creatorcontrib><creatorcontrib>Kong, Deyong</creatorcontrib><creatorcontrib>Li, Xiaoyi</creatorcontrib><creatorcontrib>Lu, Hongda</creatorcontrib><creatorcontrib>Liu, Shuiyi</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Du, Lili</creatorcontrib><creatorcontrib>Kong, Qingzhi</creatorcontrib><creatorcontrib>Huang, Xiaodong</creatorcontrib><creatorcontrib>Lu, Zhongxin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Tangwei</au><au>Chen, Weiqun</au><au>Kong, Deyong</au><au>Li, Xiaoyi</au><au>Lu, Hongda</au><au>Liu, Shuiyi</au><au>Wang, Jing</au><au>Du, Lili</au><au>Kong, Qingzhi</au><au>Huang, Xiaodong</au><au>Lu, Zhongxin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-25 targets the modulator of apoptosis 1 gene in lung cancer</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2015-08-01</date><risdate>2015</risdate><volume>36</volume><issue>8</issue><spage>925</spage><epage>935</epage><pages>925-935</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><abstract>To determine the role of miR-25 in non-small cell lung cancer (NSCLC), we first detected miR-25 expression in clinical specimens and lung cancer cell lines by quantitative real-time polymerase chain reaction. The levels of miR-25 were elevated in the plasma of NSCLC patients and NSCLC cell lines. Transfection of A549 and 95-D cells with a miR-25 inhibitor resulted in reduced cell proliferation and enhanced apoptosis. Moreover, the modulator of apoptosis 1 (MOAP1) gene was identified as a novel target of miR-25. The ability of miR-25 to promote cell proliferation and block apoptosis is attributable to its effect on MOAP1 suppression. In addition, miR-25 antagomir significantly inhibited lung cancer growth via upregulation of MOAP1 in a mouse xenograft model. Collectively, these data demonstrate that miR-25 is an important biomarker for lung cancer, and miR-25 promotes cell proliferation and inhibits apoptosis in NSCLC cells by negatively regulating MOAP1 expression.</abstract><cop>England</cop><pmid>25998847</pmid><doi>10.1093/carcin/bgv068</doi><tpages>11</tpages></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Adaptor Proteins, Signal Transducing - genetics Aged Animals Apoptosis - genetics Apoptosis Regulatory Proteins - genetics Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - pathology Case-Control Studies Cell Line, Tumor Cell Proliferation - genetics Female Gene Expression Regulation, Neoplastic Humans Lung Neoplasms - genetics Lung Neoplasms - pathology Male Mice, Inbred BALB C MicroRNAs - blood MicroRNAs - genetics Middle Aged Xenograft Model Antitumor Assays |
| title | miR-25 targets the modulator of apoptosis 1 gene in lung cancer |
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