2012
Blockade of miR-150 Maturation by MLL-Fusion/MYC/LIN-28 Is Required for MLL-Associated Leukemia
Jiang X, Huang H, Li Z, Li Y, Wang X, Gurbuxani S, Chen P, He C, You D, Zhang S, Wang J, Arnovitz S, Elkahloun A, Price C, Hong GM, Ren H, Kunjamma RB, Neilly MB, Matthews JM, Xu M, Larson RA, Le Beau MM, Slany RK, Liu PP, Lu J, Zhang J, He C, Chen J. Blockade of miR-150 Maturation by MLL-Fusion/MYC/LIN-28 Is Required for MLL-Associated Leukemia. Cancer Cell 2012, 22: 524-535. PMID: 23079661, PMCID: PMC3480215, DOI: 10.1016/j.ccr.2012.08.028.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorCell Transformation, NeoplasticDNA MethylationDown-RegulationFms-Like Tyrosine Kinase 3Gene DosageGene Expression Regulation, LeukemicHistone-Lysine N-MethyltransferaseHomeodomain ProteinsHumansLeukemiaMiceMicroRNAsMutationMyeloid Ecotropic Viral Integration Site 1 ProteinMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsNuclear ProteinsProto-Oncogene Proteins c-mycRNA-Binding ProteinsSignal TransductionConceptsMiR-150MiR-150 functionsLeukemic cell growthPathogenesis of leukemiaHoxa9/Meis1Acute leukemiaDysregulation of miRNAsExpression of microRNAsPivotal gatekeeperLeukemiaFunctional axisCell growthLeukemogenesisMYC/MLL fusion proteinsBlockadePathogenesisPosttranscriptional levelExpressionFusion proteinFLT3miR-196b directly targets both HOXA9/MEIS1 oncogenes and FAS tumour suppressor in MLL-rearranged leukaemia
Li Z, Huang H, Chen P, He M, Li Y, Arnovitz S, Jiang X, He C, Hyjek E, Zhang J, Zhang Z, Elkahloun A, Cao D, Shen C, Wunderlich M, Wang Y, Neilly MB, Jin J, Wei M, Lu J, Valk PJ, Delwel R, Lowenberg B, Le Beau MM, Vardiman J, Mulloy JC, Zeleznik-Le NJ, Liu PP, Zhang J, Chen J. miR-196b directly targets both HOXA9/MEIS1 oncogenes and FAS tumour suppressor in MLL-rearranged leukaemia. Nature Communications 2012, 3: 688. PMID: 22353710, PMCID: PMC3514459, DOI: 10.1038/ncomms1681.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBase SequenceCell Transformation, NeoplasticCells, CulturedFas ReceptorFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHematopoiesisHomeodomain ProteinsHumansLeukemia, Myeloid, AcuteMaleMiceMice, Inbred C57BLMicroRNAsMyeloid Ecotropic Viral Integration Site 1 ProteinMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsSequence Analysis, DNAConceptsMiR-196bTumor suppressorMiRNA regulation mechanismOverexpression of FASBone marrow transplantationEssential oncogenic roleMiRNA regulationEctopic expressionMixed lineage leukemiaMEIS1 expressionMLL fusionsProapoptotic genesSingle miRNACell differentiationDirect targetLeukaemic phenotypeHoxa9/Meis1Marrow transplantationNormal developmentFurther repressionLeukaemic cellsOncogenic roleLineage leukemiaNormal haematopoiesisSecondary transplantation
2009
Lin28 promotes transformation and is associated with advanced human malignancies
Viswanathan SR, Powers JT, Einhorn W, Hoshida Y, Ng TL, Toffanin S, O'Sullivan M, Lu J, Phillips LA, Lockhart VL, Shah SP, Tanwar PS, Mermel CH, Beroukhim R, Azam M, Teixeira J, Meyerson M, Hughes TP, Llovet JM, Radich J, Mullighan CG, Golub TR, Sorensen PH, Daley GQ. Lin28 promotes transformation and is associated with advanced human malignancies. Nature Genetics 2009, 41: 843-848. PMID: 19483683, PMCID: PMC2757943, DOI: 10.1038/ng.392.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinoma, HepatocellularCell Line, TumorCell Transformation, NeoplasticDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMiceMicroRNAsNeoplasmsRNA-Binding ProteinsRegulation of mir-196b by MLL and its overexpression by MLL fusions contributes to immortalization
Popovic R, Riesbeck LE, Velu CS, Chaubey A, Zhang J, Achille NJ, Erfurth FE, Eaton K, Lu J, Grimes HL, Chen J, Rowley JD, Zeleznik-Le NJ. Regulation of mir-196b by MLL and its overexpression by MLL fusions contributes to immortalization. Blood 2009, 113: 3314-3322. PMID: 19188669, PMCID: PMC2665896, DOI: 10.1182/blood-2008-04-154310.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceCell DifferentiationCell ProliferationCell Transformation, NeoplasticCells, CulturedEmbryonic Stem CellsGene Expression RegulationHistone-Lysine N-MethyltransferaseLeukemiaMiceMice, Inbred C57BLMicroRNAsMolecular Sequence DataMyeloid-Lymphoid Leukemia ProteinRecombinant Fusion ProteinsSequence Homology, Nucleic AcidUp-RegulationConceptsMLL fusion proteinsHox genesMiR-196bLeukemogenic MLL fusion proteinsFusion proteinEmbryonic stem cell differentiationStem cell differentiationDifferentiated hematopoietic cellsShort-term hematopoietic stem cellsMixed lineage leukemia (MLL) geneBone marrow progenitor cellsLeukemia developmentHOXA clusterHematopoietic stem cellsPrimary leukemia samplesChimeric proteinMarrow progenitor cellsHematopoietic lineagesCell differentiationLeukemia geneFusion contributesChromosomal translocationsHematopoietic cellsGenesStem cells
2007
Impaired microRNA processing enhances cellular transformation and tumorigenesis
Kumar MS, Lu J, Mercer KL, Golub TR, Jacks T. Impaired microRNA processing enhances cellular transformation and tumorigenesis. Nature Genetics 2007, 39: 673-677. PMID: 17401365, DOI: 10.1038/ng2003.Peer-Reviewed Original ResearchConceptsTarget mRNA transcriptsShort hairpin RNAGlobal repressionCellular transformationMRNA transcriptsMiRNA processing machinerySmall noncoding RNAsMature miRNA expressionMiRNA lossMiRNA maturationMiRNA processingMicroRNA processingNoncoding RNAsUndifferentiated stateProcessing machineryMiRNA expressionHairpin RNAConditional deletionTumorigenesisMiRNA levelsCancer cellsTumor developmentRepressionTranscriptsRNA