miR-1915 inhibits Bcl-2 to modulate multidrug resistance by increasing drug-sensitivity in human colorectal carcinoma cells
Colorectal carcinoma is a frequent cause of cancer‐related death in the world for men and women. microRNAs are endogenous small noncoding RNAs that regulate gene expression negatively at post‐transcriptional level. Here, we investigated the possible role of microRNAs in the development of multidrug...
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| Veröffentlicht in: | Molecular carcinogenesis 2013-01, Vol.52 (1), p.70-78 |
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| creator | Xu, Ke Liang, Xin Cui, Daling Wu, Yixin Shi, Weibin Liu, Jianwen |
| description | Colorectal carcinoma is a frequent cause of cancer‐related death in the world for men and women. microRNAs are endogenous small noncoding RNAs that regulate gene expression negatively at post‐transcriptional level. Here, we investigated the possible role of microRNAs in the development of multidrug resistance (MDR) in colorectal carcinoma cells. We analyzed microRNA (miRNA) expression levels between multidrug resistant colorectal carcinoma cell line HCT116/L‐OHP and its parent cell line HCT116 using a miRNA microarray. miR‐1915 had the lowest expression of miRNA in HCT116/L‐OHP cells compared to its parental cells. Overexpression of Bcl‐2 is generally associated with tumor drug resistance, meanwhile Bcl‐2 is a predicted target of miR‐1915. We found that elevated levels of miR‐1915 in the mimics‐transfected HCT116/L‐OHP cells reduced Bcl‐2 protein level and the luciferase activity of a Bcl‐2 3′‐untranslated region‐based reporter, and also sensitized these cells to some anticancer drugs. Taken together, our findings suggest that miR‐1915 could play a role in the development of MDR in colorectal carcinoma cells at least in part by modulation of apoptosis via targeting Bcl‐2. © 2011 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/mc.21832 |
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Here, we investigated the possible role of microRNAs in the development of multidrug resistance (MDR) in colorectal carcinoma cells. We analyzed microRNA (miRNA) expression levels between multidrug resistant colorectal carcinoma cell line HCT116/L‐OHP and its parent cell line HCT116 using a miRNA microarray. miR‐1915 had the lowest expression of miRNA in HCT116/L‐OHP cells compared to its parental cells. Overexpression of Bcl‐2 is generally associated with tumor drug resistance, meanwhile Bcl‐2 is a predicted target of miR‐1915. We found that elevated levels of miR‐1915 in the mimics‐transfected HCT116/L‐OHP cells reduced Bcl‐2 protein level and the luciferase activity of a Bcl‐2 3′‐untranslated region‐based reporter, and also sensitized these cells to some anticancer drugs. Taken together, our findings suggest that miR‐1915 could play a role in the development of MDR in colorectal carcinoma cells at least in part by modulation of apoptosis via targeting Bcl‐2. © 2011 Wiley Periodicals, Inc.</description><identifier>ISSN: 0899-1987</identifier><identifier>EISSN: 1098-2744</identifier><identifier>DOI: 10.1002/mc.21832</identifier><identifier>PMID: 22121083</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>3' Untranslated Regions - physiology ; Antineoplastic Agents - therapeutic use ; Apoptosis - drug effects ; Bcl-2 ; Carcinoma - drug therapy ; Cell Line, Tumor ; Cellular biology ; Chemotherapy ; Colorectal cancer ; colorectal carcinoma ; Colorectal Neoplasms - drug therapy ; Drug resistance ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Flow Cytometry ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Humans ; Membrane Potential, Mitochondrial - drug effects ; microRNA ; microRNA array ; MicroRNAs - analysis ; MicroRNAs - metabolism ; multidrug-resistance ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-bcl-2 - analysis</subject><ispartof>Molecular carcinogenesis, 2013-01, Vol.52 (1), p.70-78</ispartof><rights>Copyright © 2011 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4532-c3e6793b802d8c9283880dc8376afeefdaa3bb40be383bf398bb6cf3d01c25253</citedby><cites>FETCH-LOGICAL-c4532-c3e6793b802d8c9283880dc8376afeefdaa3bb40be383bf398bb6cf3d01c25253</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmc.21832$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmc.21832$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22121083$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Ke</creatorcontrib><creatorcontrib>Liang, Xin</creatorcontrib><creatorcontrib>Cui, Daling</creatorcontrib><creatorcontrib>Wu, Yixin</creatorcontrib><creatorcontrib>Shi, Weibin</creatorcontrib><creatorcontrib>Liu, Jianwen</creatorcontrib><title>miR-1915 inhibits Bcl-2 to modulate multidrug resistance by increasing drug-sensitivity in human colorectal carcinoma cells</title><title>Molecular carcinogenesis</title><addtitle>Mol. Carcinog</addtitle><description>Colorectal carcinoma is a frequent cause of cancer‐related death in the world for men and women. microRNAs are endogenous small noncoding RNAs that regulate gene expression negatively at post‐transcriptional level. Here, we investigated the possible role of microRNAs in the development of multidrug resistance (MDR) in colorectal carcinoma cells. We analyzed microRNA (miRNA) expression levels between multidrug resistant colorectal carcinoma cell line HCT116/L‐OHP and its parent cell line HCT116 using a miRNA microarray. miR‐1915 had the lowest expression of miRNA in HCT116/L‐OHP cells compared to its parental cells. Overexpression of Bcl‐2 is generally associated with tumor drug resistance, meanwhile Bcl‐2 is a predicted target of miR‐1915. We found that elevated levels of miR‐1915 in the mimics‐transfected HCT116/L‐OHP cells reduced Bcl‐2 protein level and the luciferase activity of a Bcl‐2 3′‐untranslated region‐based reporter, and also sensitized these cells to some anticancer drugs. 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Liang, Xin ; Cui, Daling ; Wu, Yixin ; Shi, Weibin ; Liu, Jianwen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4532-c3e6793b802d8c9283880dc8376afeefdaa3bb40be383bf398bb6cf3d01c25253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>3' Untranslated Regions - physiology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Apoptosis - drug effects</topic><topic>Bcl-2</topic><topic>Carcinoma - drug therapy</topic><topic>Cell Line, Tumor</topic><topic>Cellular biology</topic><topic>Chemotherapy</topic><topic>Colorectal cancer</topic><topic>colorectal carcinoma</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Drug resistance</topic><topic>Drug Resistance, Multiple</topic><topic>Drug Resistance, Neoplasm</topic><topic>Flow Cytometry</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Humans</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>microRNA</topic><topic>microRNA array</topic><topic>MicroRNAs - analysis</topic><topic>MicroRNAs - metabolism</topic><topic>multidrug-resistance</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Proto-Oncogene Proteins c-bcl-2 - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Ke</creatorcontrib><creatorcontrib>Liang, Xin</creatorcontrib><creatorcontrib>Cui, Daling</creatorcontrib><creatorcontrib>Wu, Yixin</creatorcontrib><creatorcontrib>Shi, Weibin</creatorcontrib><creatorcontrib>Liu, Jianwen</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular carcinogenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Ke</au><au>Liang, Xin</au><au>Cui, Daling</au><au>Wu, Yixin</au><au>Shi, Weibin</au><au>Liu, Jianwen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-1915 inhibits Bcl-2 to modulate multidrug resistance by increasing drug-sensitivity in human colorectal carcinoma cells</atitle><jtitle>Molecular carcinogenesis</jtitle><addtitle>Mol. Carcinog</addtitle><date>2013-01</date><risdate>2013</risdate><volume>52</volume><issue>1</issue><spage>70</spage><epage>78</epage><pages>70-78</pages><issn>0899-1987</issn><eissn>1098-2744</eissn><abstract>Colorectal carcinoma is a frequent cause of cancer‐related death in the world for men and women. microRNAs are endogenous small noncoding RNAs that regulate gene expression negatively at post‐transcriptional level. Here, we investigated the possible role of microRNAs in the development of multidrug resistance (MDR) in colorectal carcinoma cells. We analyzed microRNA (miRNA) expression levels between multidrug resistant colorectal carcinoma cell line HCT116/L‐OHP and its parent cell line HCT116 using a miRNA microarray. miR‐1915 had the lowest expression of miRNA in HCT116/L‐OHP cells compared to its parental cells. Overexpression of Bcl‐2 is generally associated with tumor drug resistance, meanwhile Bcl‐2 is a predicted target of miR‐1915. 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| subjects | 3' Untranslated Regions - physiology Antineoplastic Agents - therapeutic use Apoptosis - drug effects Bcl-2 Carcinoma - drug therapy Cell Line, Tumor Cellular biology Chemotherapy Colorectal cancer colorectal carcinoma Colorectal Neoplasms - drug therapy Drug resistance Drug Resistance, Multiple Drug Resistance, Neoplasm Flow Cytometry Gene expression Gene Expression Regulation, Neoplastic - drug effects Humans Membrane Potential, Mitochondrial - drug effects microRNA microRNA array MicroRNAs - analysis MicroRNAs - metabolism multidrug-resistance Oligonucleotide Array Sequence Analysis Proto-Oncogene Proteins c-bcl-2 - analysis |
| title | miR-1915 inhibits Bcl-2 to modulate multidrug resistance by increasing drug-sensitivity in human colorectal carcinoma cells |
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