Effect of miR-21 and miR-30b/c on TRAIL-induced apoptosis in glioma cells
Glioblastoma is the most frequent brain tumor in adults and is the most lethal form of human cancer. Despite the improvements in treatments, survival of patients remains poor. To define novel pathways that regulate susceptibility to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in...
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| Veröffentlicht in: | Oncogene 2013-08, Vol.32 (34), p.4001-4008 |
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| creator | Quintavalle, C Donnarumma, E Iaboni, M Roscigno, G Garofalo, M Romano, G Fiore, D De Marinis, P Croce, C M Condorelli, G |
| description | Glioblastoma is the most frequent brain tumor in adults and is the most lethal form of human cancer. Despite the improvements in treatments, survival of patients remains poor. To define novel pathways that regulate susceptibility to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in glioma, we have performed genome-wide expression profiling of microRNAs (miRs). We show that in TRAIL-resistant glioma cells, levels of different miRs are increased, and in particular, miR-30b/c and -21. We demonstrate that these miRs impair TRAIL-dependent apoptosis by inhibiting the expression of key functional proteins. T98G-sensitive cells treated with miR-21 or -30b/c become resistant to TRAIL. Furthermore, we demonstrate that miR-30b/c and miR-21 target respectively the 3′ untranslated region of caspase-3 and TAp63 mRNAs, and that those proteins mediate some of the effects of miR-30 and -21 on TRAIL resistance, even in human glioblastoma primary cells and in lung cancer cells. In conclusion, we show that high expression levels of miR-21 and -30b/c are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets for TRAIL resistance in glioma. |
| doi_str_mv | 10.1038/onc.2012.410 |
| format | Article |
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Despite the improvements in treatments, survival of patients remains poor. To define novel pathways that regulate susceptibility to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in glioma, we have performed genome-wide expression profiling of microRNAs (miRs). We show that in TRAIL-resistant glioma cells, levels of different miRs are increased, and in particular, miR-30b/c and -21. We demonstrate that these miRs impair TRAIL-dependent apoptosis by inhibiting the expression of key functional proteins. T98G-sensitive cells treated with miR-21 or -30b/c become resistant to TRAIL. Furthermore, we demonstrate that miR-30b/c and miR-21 target respectively the 3′ untranslated region of caspase-3 and TAp63 mRNAs, and that those proteins mediate some of the effects of miR-30 and -21 on TRAIL resistance, even in human glioblastoma primary cells and in lung cancer cells. In conclusion, we show that high expression levels of miR-21 and -30b/c are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets for TRAIL resistance in glioma.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2012.410</identifier><identifier>PMID: 22964638</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>3' Untranslated regions ; 3' Untranslated Regions - genetics ; Apoptosis ; Apoptosis - drug effects ; Blotting, Northern ; Blotting, Western ; Brain cancer ; Brain tumors ; Care and treatment ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Caspase-3 ; Cell Biology ; Cell Line, Tumor ; Cytokines ; Drug Resistance, Neoplasm - genetics ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Genomes ; Glioblastoma ; Glioblastoma multiforme ; Glioma ; Glioma - genetics ; Glioma - metabolism ; Glioma - pathology ; Glioma cells ; Health aspects ; HEK293 Cells ; Human Genetics ; Humans ; Internal Medicine ; Lung cancer ; Medicine ; Medicine & Public Health ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Oligonucleotide Array Sequence Analysis ; Oncology ; original-article ; Phenotypes ; Proteins ; Reverse Transcriptase Polymerase Chain Reaction ; Therapeutic targets ; TNF-Related Apoptosis-Inducing Ligand - pharmacology ; TRAIL protein ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Tumor Cells, Cultured ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism</subject><ispartof>Oncogene, 2013-08, Vol.32 (34), p.4001-4008</ispartof><rights>Macmillan Publishers Limited 2013</rights><rights>COPYRIGHT 2013 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Aug 22, 2013</rights><rights>Macmillan Publishers Limited 2013.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c589t-700ba8e585cf89dd4141a33092bd6ae694567aaaf389b64b455a38293b94d2823</citedby><cites>FETCH-LOGICAL-c589t-700ba8e585cf89dd4141a33092bd6ae694567aaaf389b64b455a38293b94d2823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2012.410$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2012.410$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22964638$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Quintavalle, C</creatorcontrib><creatorcontrib>Donnarumma, E</creatorcontrib><creatorcontrib>Iaboni, M</creatorcontrib><creatorcontrib>Roscigno, G</creatorcontrib><creatorcontrib>Garofalo, M</creatorcontrib><creatorcontrib>Romano, G</creatorcontrib><creatorcontrib>Fiore, D</creatorcontrib><creatorcontrib>De Marinis, P</creatorcontrib><creatorcontrib>Croce, C M</creatorcontrib><creatorcontrib>Condorelli, G</creatorcontrib><title>Effect of miR-21 and miR-30b/c on TRAIL-induced apoptosis in glioma cells</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Glioblastoma is the most frequent brain tumor in adults and is the most lethal form of human cancer. Despite the improvements in treatments, survival of patients remains poor. To define novel pathways that regulate susceptibility to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in glioma, we have performed genome-wide expression profiling of microRNAs (miRs). We show that in TRAIL-resistant glioma cells, levels of different miRs are increased, and in particular, miR-30b/c and -21. We demonstrate that these miRs impair TRAIL-dependent apoptosis by inhibiting the expression of key functional proteins. T98G-sensitive cells treated with miR-21 or -30b/c become resistant to TRAIL. Furthermore, we demonstrate that miR-30b/c and miR-21 target respectively the 3′ untranslated region of caspase-3 and TAp63 mRNAs, and that those proteins mediate some of the effects of miR-30 and -21 on TRAIL resistance, even in human glioblastoma primary cells and in lung cancer cells. In conclusion, we show that high expression levels of miR-21 and -30b/c are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets for TRAIL resistance in glioma.</description><subject>3' Untranslated regions</subject><subject>3' Untranslated Regions - genetics</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Blotting, Northern</subject><subject>Blotting, Western</subject><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Care and treatment</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cytokines</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Glioblastoma</subject><subject>Glioblastoma multiforme</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>Health aspects</subject><subject>HEK293 Cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Lung cancer</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Oncology</subject><subject>original-article</subject><subject>Phenotypes</subject><subject>Proteins</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Therapeutic targets</subject><subject>TNF-Related Apoptosis-Inducing Ligand - pharmacology</subject><subject>TRAIL protein</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - 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Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Quintavalle, C</au><au>Donnarumma, E</au><au>Iaboni, M</au><au>Roscigno, G</au><au>Garofalo, M</au><au>Romano, G</au><au>Fiore, D</au><au>De Marinis, P</au><au>Croce, C M</au><au>Condorelli, G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of miR-21 and miR-30b/c on TRAIL-induced apoptosis in glioma cells</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2013-08-22</date><risdate>2013</risdate><volume>32</volume><issue>34</issue><spage>4001</spage><epage>4008</epage><pages>4001-4008</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Glioblastoma is the most frequent brain tumor in adults and is the most lethal form of human cancer. Despite the improvements in treatments, survival of patients remains poor. To define novel pathways that regulate susceptibility to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in glioma, we have performed genome-wide expression profiling of microRNAs (miRs). We show that in TRAIL-resistant glioma cells, levels of different miRs are increased, and in particular, miR-30b/c and -21. We demonstrate that these miRs impair TRAIL-dependent apoptosis by inhibiting the expression of key functional proteins. T98G-sensitive cells treated with miR-21 or -30b/c become resistant to TRAIL. Furthermore, we demonstrate that miR-30b/c and miR-21 target respectively the 3′ untranslated region of caspase-3 and TAp63 mRNAs, and that those proteins mediate some of the effects of miR-30 and -21 on TRAIL resistance, even in human glioblastoma primary cells and in lung cancer cells. In conclusion, we show that high expression levels of miR-21 and -30b/c are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets for TRAIL resistance in glioma.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>22964638</pmid><doi>10.1038/onc.2012.410</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncogene, 2013-08, Vol.32 (34), p.4001-4008 |
| issn | 0950-9232 1476-5594 |
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| source | MEDLINE; SpringerLink Journals; Nature Journals Online; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | 3' Untranslated regions 3' Untranslated Regions - genetics Apoptosis Apoptosis - drug effects Blotting, Northern Blotting, Western Brain cancer Brain tumors Care and treatment Caspase 3 - genetics Caspase 3 - metabolism Caspase-3 Cell Biology Cell Line, Tumor Cytokines Drug Resistance, Neoplasm - genetics Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic Genetic aspects Genomes Glioblastoma Glioblastoma multiforme Glioma Glioma - genetics Glioma - metabolism Glioma - pathology Glioma cells Health aspects HEK293 Cells Human Genetics Humans Internal Medicine Lung cancer Medicine Medicine & Public Health MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Oligonucleotide Array Sequence Analysis Oncology original-article Phenotypes Proteins Reverse Transcriptase Polymerase Chain Reaction Therapeutic targets TNF-Related Apoptosis-Inducing Ligand - pharmacology TRAIL protein Transcription Factors - genetics Transcription Factors - metabolism Tumor Cells, Cultured Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism |
| title | Effect of miR-21 and miR-30b/c on TRAIL-induced apoptosis in glioma cells |
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