2012
miR-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
2010
Aberrant overexpression and function of the miR-17-92 cluster in MLL-rearranged acute leukemia
Mi S, Li Z, Chen P, He C, Cao D, Elkahloun A, Lu J, Pelloso LA, Wunderlich M, Huang H, Luo RT, Sun M, He M, Neilly MB, Zeleznik-Le NJ, Thirman MJ, Mulloy JC, Liu PP, Rowley JD, Chen J. Aberrant overexpression and function of the miR-17-92 cluster in MLL-rearranged acute leukemia. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 3710-3715. PMID: 20133587, PMCID: PMC2840429, DOI: 10.1073/pnas.0914900107.Peer-Reviewed Original ResearchConceptsMouse bone marrow progenitor cellsMiRNA clusterTarget genesMLL fusionsBone marrow progenitor cellsMiR-17Marrow progenitor cellsCell differentiationDNA copy number amplificationsWild-type MLLProgenitor cellsRelevant target genesHistone H3 acetylationPotential target genesMLL fusion genesCopy number amplificationDevelopment of MLLH3K4 trimethylationIndividual miRNAsH3 acetylationMixed lineage leukemiaCell cycleHuman cellsDirect bindingMiRNAs
2009
Regulation 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