Upregulation of the miR-212/132 cluster suppresses proliferation of human lung cancer cells
Lung cancer is the leading cause of cancer-related mortality worldwide. microRNAs (miRNAs) are small post-transcriptional regulatory non-coding RNAs that function as oncogenes or tumor suppressors in human cancers. Emerging evidence reveals that deregulation of miRNAs contributes to the progression...
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| Veröffentlicht in: | Oncology reports 2015-02, Vol.33 (2), p.705-712 |
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| creator | JIANG, XIN CHEN, XIALIN CHEN, LING MA, YAN ZHOU, LINYAN QI, QIUFENG LIU, YONGPING ZHANG, SHUYU LUO, JUDONG ZHOU, XIFA |
| description | Lung cancer is the leading cause of cancer-related mortality worldwide. microRNAs (miRNAs) are small post-transcriptional regulatory non-coding RNAs that function as oncogenes or tumor suppressors in human cancers. Emerging evidence reveals that deregulation of miRNAs contributes to the progression of human lung cancer, which is the leading cause of cancer-related deaths worldwide. In the present study, we found that upregulation of the miR-212/132 cluster significantly suppressed the growth and focus formation of A549 and H1299 cells. Moreover, forced expression of this cluster conferred radiosensitivity and inhibited the migration of lung cancer cells, whereas downregulation of miR-212/132 reversed the above effects. Furthermore, miR-212/132 overexpression induced cell cycle arrest at the G1/S phase transition of the lung cancer cells, and inhibition of miR-132 and miR-212 abrogated this arrest. In addition, miR-212/132 overexpression increased the percentage of cells undergoing apoptosis. Cells transfected with the miR-212/132 cluster exhibited upregulated p21 expression and reduced cyclin D1 expression. Conversely, cells transfected with the miR-212/132 inhibitor showed reduced expression of p21 and upregulated expression of cyclin D1, suggesting that miR-212/132 may mediate proliferation and cell cycle arrest through p21 and cyclin D1. Our study provides insight into the biological function of the miR-212/132 cluster in lung cancer. The present study may provide a potential therapeutic target for the treatment of lung cancer. |
| doi_str_mv | 10.3892/or.2014.3637 |
| format | Article |
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Emerging evidence reveals that deregulation of miRNAs contributes to the progression of human lung cancer, which is the leading cause of cancer-related deaths worldwide. In the present study, we found that upregulation of the miR-212/132 cluster significantly suppressed the growth and focus formation of A549 and H1299 cells. Moreover, forced expression of this cluster conferred radiosensitivity and inhibited the migration of lung cancer cells, whereas downregulation of miR-212/132 reversed the above effects. Furthermore, miR-212/132 overexpression induced cell cycle arrest at the G1/S phase transition of the lung cancer cells, and inhibition of miR-132 and miR-212 abrogated this arrest. In addition, miR-212/132 overexpression increased the percentage of cells undergoing apoptosis. Cells transfected with the miR-212/132 cluster exhibited upregulated p21 expression and reduced cyclin D1 expression. Conversely, cells transfected with the miR-212/132 inhibitor showed reduced expression of p21 and upregulated expression of cyclin D1, suggesting that miR-212/132 may mediate proliferation and cell cycle arrest through p21 and cyclin D1. Our study provides insight into the biological function of the miR-212/132 cluster in lung cancer. The present study may provide a potential therapeutic target for the treatment of lung cancer.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2014.3637</identifier><identifier>PMID: 25435090</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Apoptosis ; Cancer ; Cancer cells ; Cancer therapies ; Cell cycle ; Cell Cycle Checkpoints ; Cell division ; Cell Line, Tumor ; Cell Movement - radiation effects ; Cyclin D1 - metabolism ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Development and progression ; Gene Expression Regulation, Neoplastic ; Health aspects ; Humans ; Lung cancer ; Lung Neoplasms - metabolism ; Lung Neoplasms - radiotherapy ; MicroRNA ; MicroRNAs - metabolism ; miR-212/132 ; Mortality ; Oncology, Experimental ; Pancreatic cancer ; Phase transitions ; Physiological aspects ; Plasmids ; proliferation ; radiosensitivity ; Roles ; Studies</subject><ispartof>Oncology reports, 2015-02, Vol.33 (2), p.705-712</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-2540be20869b96ca0c42a3577efb354a8fddab47c2c7f00ad91346fa587fa6093</citedby><cites>FETCH-LOGICAL-c486t-2540be20869b96ca0c42a3577efb354a8fddab47c2c7f00ad91346fa587fa6093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25435090$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JIANG, XIN</creatorcontrib><creatorcontrib>CHEN, XIALIN</creatorcontrib><creatorcontrib>CHEN, LING</creatorcontrib><creatorcontrib>MA, YAN</creatorcontrib><creatorcontrib>ZHOU, LINYAN</creatorcontrib><creatorcontrib>QI, QIUFENG</creatorcontrib><creatorcontrib>LIU, YONGPING</creatorcontrib><creatorcontrib>ZHANG, SHUYU</creatorcontrib><creatorcontrib>LUO, JUDONG</creatorcontrib><creatorcontrib>ZHOU, XIFA</creatorcontrib><title>Upregulation of the miR-212/132 cluster suppresses proliferation of human lung cancer cells</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Lung cancer is the leading cause of cancer-related mortality worldwide. microRNAs (miRNAs) are small post-transcriptional regulatory non-coding RNAs that function as oncogenes or tumor suppressors in human cancers. Emerging evidence reveals that deregulation of miRNAs contributes to the progression of human lung cancer, which is the leading cause of cancer-related deaths worldwide. In the present study, we found that upregulation of the miR-212/132 cluster significantly suppressed the growth and focus formation of A549 and H1299 cells. Moreover, forced expression of this cluster conferred radiosensitivity and inhibited the migration of lung cancer cells, whereas downregulation of miR-212/132 reversed the above effects. Furthermore, miR-212/132 overexpression induced cell cycle arrest at the G1/S phase transition of the lung cancer cells, and inhibition of miR-132 and miR-212 abrogated this arrest. In addition, miR-212/132 overexpression increased the percentage of cells undergoing apoptosis. Cells transfected with the miR-212/132 cluster exhibited upregulated p21 expression and reduced cyclin D1 expression. Conversely, cells transfected with the miR-212/132 inhibitor showed reduced expression of p21 and upregulated expression of cyclin D1, suggesting that miR-212/132 may mediate proliferation and cell cycle arrest through p21 and cyclin D1. Our study provides insight into the biological function of the miR-212/132 cluster in lung cancer. The present study may provide a potential therapeutic target for the treatment of lung cancer.</description><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints</subject><subject>Cell division</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - radiation effects</subject><subject>Cyclin D1 - metabolism</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>Development and progression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - radiotherapy</subject><subject>MicroRNA</subject><subject>MicroRNAs - metabolism</subject><subject>miR-212/132</subject><subject>Mortality</subject><subject>Oncology, Experimental</subject><subject>Pancreatic cancer</subject><subject>Phase transitions</subject><subject>Physiological aspects</subject><subject>Plasmids</subject><subject>proliferation</subject><subject>radiosensitivity</subject><subject>Roles</subject><subject>Studies</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptks1rFTEUxQdRbK3uXMuAIC6c15uvyWRZil9QEMSC4CJkMsl7KZlkTCYL_3sztL5akSwSwu_cnHtPmuYlgh0ZBD6PaYcB0R3pCX_UnCIuUIcpQY_rGTDqCGHfT5pnOd8AYA69eNqcYEYJAwGnzY_rJZl98Wp1MbTRtuvBtLP72mGEzxHBrfYlrya1uSyVzNnkdknRO2vSUXMoswqtL2HfahV0pbXxPj9vnljls3lxt5811x_ef7v81F19-fj58uKq03To166agdFgGHoxil4r0BQrwjg3diSMqsFOkxop11hzC6AmgQjtrWIDt6oHQc6at7d1q7GfxeRVzi5vDlQwsWSJeiLEQBlBFX39D3oTSwrVnUSCEOAIEbin9sob6YKNa1J6KyovKCABDBiv1O4_VF2TmZ2OwVhX7x8I3vwlOBjl10OOvmxjzA_Bd7egTjHnZKxckptV-iURyC10GZPcQpdb6BV_dddUGWczHeE_Kd8_nBcVJjfFfGRiqh-kA9wBB0Z-A-3ksB8</recordid><startdate>20150201</startdate><enddate>20150201</enddate><creator>JIANG, XIN</creator><creator>CHEN, XIALIN</creator><creator>CHEN, LING</creator><creator>MA, YAN</creator><creator>ZHOU, LINYAN</creator><creator>QI, QIUFENG</creator><creator>LIU, YONGPING</creator><creator>ZHANG, SHUYU</creator><creator>LUO, JUDONG</creator><creator>ZHOU, XIFA</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20150201</creationdate><title>Upregulation of the miR-212/132 cluster suppresses proliferation of human lung cancer cells</title><author>JIANG, XIN ; CHEN, XIALIN ; CHEN, LING ; MA, YAN ; ZHOU, LINYAN ; QI, QIUFENG ; LIU, YONGPING ; ZHANG, SHUYU ; LUO, JUDONG ; ZHOU, XIFA</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-2540be20869b96ca0c42a3577efb354a8fddab47c2c7f00ad91346fa587fa6093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints</topic><topic>Cell division</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - radiation effects</topic><topic>Cyclin D1 - metabolism</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>Development and progression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - radiotherapy</topic><topic>MicroRNA</topic><topic>MicroRNAs - metabolism</topic><topic>miR-212/132</topic><topic>Mortality</topic><topic>Oncology, Experimental</topic><topic>Pancreatic cancer</topic><topic>Phase transitions</topic><topic>Physiological aspects</topic><topic>Plasmids</topic><topic>proliferation</topic><topic>radiosensitivity</topic><topic>Roles</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>JIANG, XIN</creatorcontrib><creatorcontrib>CHEN, XIALIN</creatorcontrib><creatorcontrib>CHEN, LING</creatorcontrib><creatorcontrib>MA, YAN</creatorcontrib><creatorcontrib>ZHOU, LINYAN</creatorcontrib><creatorcontrib>QI, QIUFENG</creatorcontrib><creatorcontrib>LIU, YONGPING</creatorcontrib><creatorcontrib>ZHANG, SHUYU</creatorcontrib><creatorcontrib>LUO, JUDONG</creatorcontrib><creatorcontrib>ZHOU, XIFA</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>JIANG, XIN</au><au>CHEN, XIALIN</au><au>CHEN, LING</au><au>MA, YAN</au><au>ZHOU, LINYAN</au><au>QI, QIUFENG</au><au>LIU, YONGPING</au><au>ZHANG, SHUYU</au><au>LUO, JUDONG</au><au>ZHOU, XIFA</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of the miR-212/132 cluster suppresses proliferation of human lung cancer cells</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2015-02-01</date><risdate>2015</risdate><volume>33</volume><issue>2</issue><spage>705</spage><epage>712</epage><pages>705-712</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Lung cancer is the leading cause of cancer-related mortality worldwide. microRNAs (miRNAs) are small post-transcriptional regulatory non-coding RNAs that function as oncogenes or tumor suppressors in human cancers. Emerging evidence reveals that deregulation of miRNAs contributes to the progression of human lung cancer, which is the leading cause of cancer-related deaths worldwide. In the present study, we found that upregulation of the miR-212/132 cluster significantly suppressed the growth and focus formation of A549 and H1299 cells. Moreover, forced expression of this cluster conferred radiosensitivity and inhibited the migration of lung cancer cells, whereas downregulation of miR-212/132 reversed the above effects. Furthermore, miR-212/132 overexpression induced cell cycle arrest at the G1/S phase transition of the lung cancer cells, and inhibition of miR-132 and miR-212 abrogated this arrest. In addition, miR-212/132 overexpression increased the percentage of cells undergoing apoptosis. Cells transfected with the miR-212/132 cluster exhibited upregulated p21 expression and reduced cyclin D1 expression. Conversely, cells transfected with the miR-212/132 inhibitor showed reduced expression of p21 and upregulated expression of cyclin D1, suggesting that miR-212/132 may mediate proliferation and cell cycle arrest through p21 and cyclin D1. Our study provides insight into the biological function of the miR-212/132 cluster in lung cancer. The present study may provide a potential therapeutic target for the treatment of lung cancer.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25435090</pmid><doi>10.3892/or.2014.3637</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Cancer Cancer cells Cancer therapies Cell cycle Cell Cycle Checkpoints Cell division Cell Line, Tumor Cell Movement - radiation effects Cyclin D1 - metabolism Cyclin-Dependent Kinase Inhibitor p21 - metabolism Development and progression Gene Expression Regulation, Neoplastic Health aspects Humans Lung cancer Lung Neoplasms - metabolism Lung Neoplasms - radiotherapy MicroRNA MicroRNAs - metabolism miR-212/132 Mortality Oncology, Experimental Pancreatic cancer Phase transitions Physiological aspects Plasmids proliferation radiosensitivity Roles Studies |
| title | Upregulation of the miR-212/132 cluster suppresses proliferation of human lung cancer cells |
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