The microRNA-302b-inhibited insulin-like growth factor-binding protein 2 signaling pathway induces glioma cell apoptosis by targeting nuclear factor IA
MicroRNAs are small noncoding RNAs that post-transcriptionally control the expression of genes involved in glioblastoma multiforme (GBM) development. Although miR-302b functions as a tumor suppressor, its role in GBM is still unclear. Therefore, this study comprehensively explored the roles of miR-3...
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description | MicroRNAs are small noncoding RNAs that post-transcriptionally control the expression of genes involved in glioblastoma multiforme (GBM) development. Although miR-302b functions as a tumor suppressor, its role in GBM is still unclear. Therefore, this study comprehensively explored the roles of miR-302b-mediated gene networks in GBM cell death. We found that miR-302b levels were significantly higher in primary astrocytes than in GBM cell lines. miR-302b overexpression dose dependently reduced U87-MG cell viability and induced apoptosis through caspase-3 activation and poly(ADP ribose) polymerase degradation. A transcriptome microarray revealed 150 downregulated genes and 380 upregulated genes in miR-302b-overexpressing cells. Nuclear factor IA (NFIA), higher levels of which were significantly related to poor survival, was identified as a direct target gene of miR-302b and was involved in miR-302b-induced glioma cell death. Higher NFIA levels were observed in GBM cell lines and human tumor sections compared with astrocytes and non-tumor tissues, respectively. NFIA knockdown significantly enhanced apoptosis. We found high levels of insulin-like growth factor-binding protein 2 (IGFBP2), another miR-302b-downregulated gene, in patients with poor survival. We verified that NFIA binds to the IGFBP2 promoter and transcriptionally enhances IGFBP2 expression levels. We identified that NFIA-mediated IGFBP2 signaling pathways are involved in miR-302b-induced glioma cell death. The identification of a regulatory loop whereby miR-302b inhibits NFIA, leading to a decrease in expression of IGFBP-2, may provide novel directions for developing therapies to target glioblastoma tumorigenesis. |
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Although miR-302b functions as a tumor suppressor, its role in GBM is still unclear. Therefore, this study comprehensively explored the roles of miR-302b-mediated gene networks in GBM cell death. We found that miR-302b levels were significantly higher in primary astrocytes than in GBM cell lines. miR-302b overexpression dose dependently reduced U87-MG cell viability and induced apoptosis through caspase-3 activation and poly(ADP ribose) polymerase degradation. A transcriptome microarray revealed 150 downregulated genes and 380 upregulated genes in miR-302b-overexpressing cells. Nuclear factor IA (NFIA), higher levels of which were significantly related to poor survival, was identified as a direct target gene of miR-302b and was involved in miR-302b-induced glioma cell death. Higher NFIA levels were observed in GBM cell lines and human tumor sections compared with astrocytes and non-tumor tissues, respectively. NFIA knockdown significantly enhanced apoptosis. We found high levels of insulin-like growth factor-binding protein 2 (IGFBP2), another miR-302b-downregulated gene, in patients with poor survival. We verified that NFIA binds to the IGFBP2 promoter and transcriptionally enhances IGFBP2 expression levels. We identified that NFIA-mediated IGFBP2 signaling pathways are involved in miR-302b-induced glioma cell death. The identification of a regulatory loop whereby miR-302b inhibits NFIA, leading to a decrease in expression of IGFBP-2, may provide novel directions for developing therapies to target glioblastoma tumorigenesis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0173890</identifier><identifier>PMID: 28323865</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenosine diphosphate ; Apoptosis ; Apoptosis - genetics ; Apoptosis - physiology ; Astrocytes ; Astrocytes - cytology ; Astrocytes - metabolism ; Biochemistry ; Biology ; Biology and Life Sciences ; Biotechnology ; Breast cancer ; Caspase ; Caspase-3 ; Cell culture ; Cell death ; Cell growth ; Cell Line, Tumor ; Cell Survival - genetics ; DNA microarrays ; Down-Regulation ; Gene expression ; Gene Knockdown Techniques ; Gene Regulatory Networks ; Genes ; Genetic aspects ; Genomics ; Glioblastoma ; Glioblastoma - genetics ; Glioblastoma - metabolism ; Glioblastoma - pathology ; Glioblastoma multiforme ; Glioblastomas ; Glioma ; Glioma - genetics ; Glioma - metabolism ; Glioma - pathology ; Glioma cells ; Humans ; Immunoglobulins ; Insulin ; Insulin-Like Growth Factor Binding Protein 2 - antagonists & inhibitors ; Insulin-Like Growth Factor Binding Protein 2 - genetics ; Insulin-Like Growth Factor Binding Protein 2 - metabolism ; Insulin-like growth factor I ; Insulin-like growth factor-binding protein 2 ; Insulin-like growth factors ; Kinases ; Medical research ; Medicine ; Medicine and Health Sciences ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Mortality ; NFI Transcription Factors - antagonists & inhibitors ; NFI Transcription Factors - genetics ; NFI Transcription Factors - metabolism ; Pharmacy ; Post-transcription ; Promoter Regions, Genetic ; Proteins ; Research and Analysis Methods ; Ribonucleic acid ; Ribose ; RNA ; Signal Transduction ; Signaling ; Stem cells ; Survival ; Target recognition ; Tissues ; Transcription factors ; Transcriptome ; Tumor cell lines ; Tumor suppressor genes ; Tumorigenesis</subject><ispartof>PloS one, 2017-03, Vol.12 (3), p.e0173890-e0173890</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Lee et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Lee et al 2017 Lee et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-1af328dee0b764f20530093e012d90d489e2e31c3e1d87e21b333d6b5711c8423</citedby><cites>FETCH-LOGICAL-c725t-1af328dee0b764f20530093e012d90d489e2e31c3e1d87e21b333d6b5711c8423</cites><orcidid>0000-0002-4696-3924</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5360322/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5360322/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28323865$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ulasov, Ilya</contributor><creatorcontrib>Lee, Chin-Cheng</creatorcontrib><creatorcontrib>Chen, Peng-Hsu</creatorcontrib><creatorcontrib>Ho, Kuo-Hao</creatorcontrib><creatorcontrib>Shih, Chwen-Ming</creatorcontrib><creatorcontrib>Cheng, Chia-Hsiung</creatorcontrib><creatorcontrib>Lin, Cheng-Wei</creatorcontrib><creatorcontrib>Cheng, Kur-Ta</creatorcontrib><creatorcontrib>Liu, Ann-Jeng</creatorcontrib><creatorcontrib>Chen, Ku-Chung</creatorcontrib><title>The microRNA-302b-inhibited insulin-like growth factor-binding protein 2 signaling pathway induces glioma cell apoptosis by targeting nuclear factor IA</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>MicroRNAs are small noncoding RNAs that post-transcriptionally control the expression of genes involved in glioblastoma multiforme (GBM) development. Although miR-302b functions as a tumor suppressor, its role in GBM is still unclear. Therefore, this study comprehensively explored the roles of miR-302b-mediated gene networks in GBM cell death. We found that miR-302b levels were significantly higher in primary astrocytes than in GBM cell lines. miR-302b overexpression dose dependently reduced U87-MG cell viability and induced apoptosis through caspase-3 activation and poly(ADP ribose) polymerase degradation. A transcriptome microarray revealed 150 downregulated genes and 380 upregulated genes in miR-302b-overexpressing cells. Nuclear factor IA (NFIA), higher levels of which were significantly related to poor survival, was identified as a direct target gene of miR-302b and was involved in miR-302b-induced glioma cell death. Higher NFIA levels were observed in GBM cell lines and human tumor sections compared with astrocytes and non-tumor tissues, respectively. NFIA knockdown significantly enhanced apoptosis. We found high levels of insulin-like growth factor-binding protein 2 (IGFBP2), another miR-302b-downregulated gene, in patients with poor survival. We verified that NFIA binds to the IGFBP2 promoter and transcriptionally enhances IGFBP2 expression levels. We identified that NFIA-mediated IGFBP2 signaling pathways are involved in miR-302b-induced glioma cell death. The identification of a regulatory loop whereby miR-302b inhibits NFIA, leading to a decrease in expression of IGFBP-2, may provide novel directions for developing therapies to target glioblastoma tumorigenesis.</description><subject>Adenosine diphosphate</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis - physiology</subject><subject>Astrocytes</subject><subject>Astrocytes - cytology</subject><subject>Astrocytes - metabolism</subject><subject>Biochemistry</subject><subject>Biology</subject><subject>Biology and Life Sciences</subject><subject>Biotechnology</subject><subject>Breast cancer</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell culture</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - genetics</subject><subject>DNA microarrays</subject><subject>Down-Regulation</subject><subject>Gene expression</subject><subject>Gene Knockdown Techniques</subject><subject>Gene Regulatory Networks</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genomics</subject><subject>Glioblastoma</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - metabolism</subject><subject>Glioblastoma - pathology</subject><subject>Glioblastoma multiforme</subject><subject>Glioblastomas</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Insulin</subject><subject>Insulin-Like Growth Factor Binding Protein 2 - antagonists & inhibitors</subject><subject>Insulin-Like Growth Factor Binding Protein 2 - genetics</subject><subject>Insulin-Like Growth Factor Binding Protein 2 - metabolism</subject><subject>Insulin-like growth factor I</subject><subject>Insulin-like growth factor-binding protein 2</subject><subject>Insulin-like growth factors</subject><subject>Kinases</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Mortality</subject><subject>NFI Transcription Factors - antagonists & inhibitors</subject><subject>NFI Transcription Factors - genetics</subject><subject>NFI Transcription Factors - metabolism</subject><subject>Pharmacy</subject><subject>Post-transcription</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>Ribonucleic acid</subject><subject>Ribose</subject><subject>RNA</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Stem cells</subject><subject>Survival</subject><subject>Target recognition</subject><subject>Tissues</subject><subject>Transcription factors</subject><subject>Transcriptome</subject><subject>Tumor cell lines</subject><subject>Tumor suppressor genes</subject><subject>Tumorigenesis</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk9tu1DAQhiMEoqXwBggiISG4yOJTEucGaVVxWKmiUincWk48Sbxk7a3tUPokvC5Om1a7qBdVLmKNv_-f8diTJC8xWmBa4g9rOzojh8XWGlggXFJeoUfJIa4oyQqC6OOd9UHyzPs1QjnlRfE0OSCckrjMD5O_5z2kG904e_ZtmVFE6kybXtc6gEq18eOgTTboX5B2zl6GPm1lE6zLam2UNl26dTaANilJve5iOdcxGfpLeRXlamzAp92g7UamDQxDKrd2G6zXPq2v0iBdB2GSmLEZQLrZPV0tnydPWjl4eDH_j5Ifnz-dH3_NTk6_rI6XJ1lTkjxkWLaUcAWA6rJgLYknRKiigDBRFVKMV0CA4oYCVrwEgmtKqSrqvMS44YzQo-T1je92sF7MPfUC87IqEKEli8TqhlBWrsXW6Y10V8JKLa4D1nVCuqBj_SIn0KBc5rmihMXcVcyOGKlVjlgryynbxznbWG9ANWCCk8Oe6f6O0b3o7G-R0wJRMhm8mw2cvRjBB7HRfmqsNGDHqW7OK45Y7MMDUIQ4K-PLOUre_Ife34iZ6mQ8qzatjSU2k6lYMl4wRgpGI7W4h4qfgvjM4lttdYzvCd7vCSIT4E_o5Oi9WH0_ezh7-nOffbvD9iCH0Hs7jEFb4_dBdgPGIfDeQXt3HxiJadRuuyGmURPzqEXZq927vBPdzhb9B0c3I08</recordid><startdate>20170321</startdate><enddate>20170321</enddate><creator>Lee, 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microRNA-302b-inhibited insulin-like growth factor-binding protein 2 signaling pathway induces glioma cell apoptosis by targeting nuclear factor IA</title><author>Lee, Chin-Cheng ; Chen, Peng-Hsu ; Ho, Kuo-Hao ; Shih, Chwen-Ming ; Cheng, Chia-Hsiung ; Lin, Cheng-Wei ; Cheng, Kur-Ta ; Liu, Ann-Jeng ; Chen, Ku-Chung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-1af328dee0b764f20530093e012d90d489e2e31c3e1d87e21b333d6b5711c8423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenosine diphosphate</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis - physiology</topic><topic>Astrocytes</topic><topic>Astrocytes - cytology</topic><topic>Astrocytes - metabolism</topic><topic>Biochemistry</topic><topic>Biology</topic><topic>Biology and Life Sciences</topic><topic>Biotechnology</topic><topic>Breast cancer</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Cell culture</topic><topic>Cell death</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - genetics</topic><topic>DNA microarrays</topic><topic>Down-Regulation</topic><topic>Gene expression</topic><topic>Gene Knockdown Techniques</topic><topic>Gene Regulatory Networks</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genomics</topic><topic>Glioblastoma</topic><topic>Glioblastoma - genetics</topic><topic>Glioblastoma - metabolism</topic><topic>Glioblastoma - pathology</topic><topic>Glioblastoma multiforme</topic><topic>Glioblastomas</topic><topic>Glioma</topic><topic>Glioma - genetics</topic><topic>Glioma - metabolism</topic><topic>Glioma - pathology</topic><topic>Glioma cells</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Insulin</topic><topic>Insulin-Like Growth Factor Binding Protein 2 - antagonists & inhibitors</topic><topic>Insulin-Like Growth Factor Binding Protein 2 - genetics</topic><topic>Insulin-Like Growth Factor Binding Protein 2 - metabolism</topic><topic>Insulin-like growth factor I</topic><topic>Insulin-like growth factor-binding protein 2</topic><topic>Insulin-like growth factors</topic><topic>Kinases</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Mortality</topic><topic>NFI Transcription Factors - antagonists & inhibitors</topic><topic>NFI Transcription Factors - genetics</topic><topic>NFI Transcription Factors - metabolism</topic><topic>Pharmacy</topic><topic>Post-transcription</topic><topic>Promoter Regions, Genetic</topic><topic>Proteins</topic><topic>Research and Analysis Methods</topic><topic>Ribonucleic acid</topic><topic>Ribose</topic><topic>RNA</topic><topic>Signal 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Chin-Cheng</au><au>Chen, Peng-Hsu</au><au>Ho, Kuo-Hao</au><au>Shih, Chwen-Ming</au><au>Cheng, Chia-Hsiung</au><au>Lin, Cheng-Wei</au><au>Cheng, Kur-Ta</au><au>Liu, Ann-Jeng</au><au>Chen, Ku-Chung</au><au>Ulasov, Ilya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The microRNA-302b-inhibited insulin-like growth factor-binding protein 2 signaling pathway induces glioma cell apoptosis by targeting nuclear factor IA</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-03-21</date><risdate>2017</risdate><volume>12</volume><issue>3</issue><spage>e0173890</spage><epage>e0173890</epage><pages>e0173890-e0173890</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>MicroRNAs are small noncoding RNAs that post-transcriptionally control the expression of genes involved in glioblastoma multiforme (GBM) development. Although miR-302b functions as a tumor suppressor, its role in GBM is still unclear. Therefore, this study comprehensively explored the roles of miR-302b-mediated gene networks in GBM cell death. We found that miR-302b levels were significantly higher in primary astrocytes than in GBM cell lines. miR-302b overexpression dose dependently reduced U87-MG cell viability and induced apoptosis through caspase-3 activation and poly(ADP ribose) polymerase degradation. A transcriptome microarray revealed 150 downregulated genes and 380 upregulated genes in miR-302b-overexpressing cells. Nuclear factor IA (NFIA), higher levels of which were significantly related to poor survival, was identified as a direct target gene of miR-302b and was involved in miR-302b-induced glioma cell death. Higher NFIA levels were observed in GBM cell lines and human tumor sections compared with astrocytes and non-tumor tissues, respectively. NFIA knockdown significantly enhanced apoptosis. We found high levels of insulin-like growth factor-binding protein 2 (IGFBP2), another miR-302b-downregulated gene, in patients with poor survival. We verified that NFIA binds to the IGFBP2 promoter and transcriptionally enhances IGFBP2 expression levels. We identified that NFIA-mediated IGFBP2 signaling pathways are involved in miR-302b-induced glioma cell death. The identification of a regulatory loop whereby miR-302b inhibits NFIA, leading to a decrease in expression of IGFBP-2, may provide novel directions for developing therapies to target glioblastoma tumorigenesis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28323865</pmid><doi>10.1371/journal.pone.0173890</doi><tpages>e0173890</tpages><orcidid>https://orcid.org/0000-0002-4696-3924</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2017-03, Vol.12 (3), p.e0173890-e0173890 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_1879602374 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Adenosine diphosphate Apoptosis Apoptosis - genetics Apoptosis - physiology Astrocytes Astrocytes - cytology Astrocytes - metabolism Biochemistry Biology Biology and Life Sciences Biotechnology Breast cancer Caspase Caspase-3 Cell culture Cell death Cell growth Cell Line, Tumor Cell Survival - genetics DNA microarrays Down-Regulation Gene expression Gene Knockdown Techniques Gene Regulatory Networks Genes Genetic aspects Genomics Glioblastoma Glioblastoma - genetics Glioblastoma - metabolism Glioblastoma - pathology Glioblastoma multiforme Glioblastomas Glioma Glioma - genetics Glioma - metabolism Glioma - pathology Glioma cells Humans Immunoglobulins Insulin Insulin-Like Growth Factor Binding Protein 2 - antagonists & inhibitors Insulin-Like Growth Factor Binding Protein 2 - genetics Insulin-Like Growth Factor Binding Protein 2 - metabolism Insulin-like growth factor I Insulin-like growth factor-binding protein 2 Insulin-like growth factors Kinases Medical research Medicine Medicine and Health Sciences MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Mortality NFI Transcription Factors - antagonists & inhibitors NFI Transcription Factors - genetics NFI Transcription Factors - metabolism Pharmacy Post-transcription Promoter Regions, Genetic Proteins Research and Analysis Methods Ribonucleic acid Ribose RNA Signal Transduction Signaling Stem cells Survival Target recognition Tissues Transcription factors Transcriptome Tumor cell lines Tumor suppressor genes Tumorigenesis |
title | The microRNA-302b-inhibited insulin-like growth factor-binding protein 2 signaling pathway induces glioma cell apoptosis by targeting nuclear factor IA |
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