2020
KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer
Alam H, Tang M, Maitituoheti M, Dhar S, Kumar M, Han C, Ambati C, Amin S, Gu B, Chen T, Lin Y, Chen J, Muller F, Putluri N, Flores E, DeMayo F, Baseler L, Rai K, Lee M. KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer. Cancer Cell 2020, 37: 599-617.e7. PMID: 32243837, PMCID: PMC7178078, DOI: 10.1016/j.ccell.2020.03.005.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAnimalsAntimetabolitesApoptosisBiomarkers, TumorCell ProliferationDeoxyglucoseDNA-Binding ProteinsEnhancer Elements, GeneticGene Expression Regulation, NeoplasticGlycolysisHistone-Lysine N-MethyltransferaseHistonesHumansLung NeoplasmsMiceMice, KnockoutMice, NudeMutationMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsPeriod Circadian ProteinsPrognosisTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsLung cancerLung-specific lossHuman lung cancer cellsExpression of Per2Lung cancer cellsHistone methyltransferase KMT2DLung tumor suppressorTumor suppressive roleMultiple glycolytic genesLung tumorigenesisEpigenetic modifiersPharmacological inhibitionTherapeutic vulnerabilitiesGlycolytic inhibitorCancerCancer cellsKMT2DFunction mutationsTumor suppressorPer2GlycolysisGlycolytic genesMutationsMice
2019
p53 Is a Master Regulator of Proteostasis in SMARCB1-Deficient Malignant Rhabdoid Tumors
Carugo A, Minelli R, Sapio L, Soeung M, Carbone F, Robinson F, Tepper J, Chen Z, Lovisa S, Svelto M, Amin S, Srinivasan S, Del Poggetto E, Loponte S, Puca F, Dey P, Malouf G, Su X, Li L, Lopez-Terrada D, Rakheja D, Lazar A, Netto G, Rao P, Sgambato A, Maitra A, Tripathi D, Walker C, Karam J, Heffernan T, Viale A, Roberts C, Msaouel P, Tannir N, Draetta G, Genovese G. p53 Is a Master Regulator of Proteostasis in SMARCB1-Deficient Malignant Rhabdoid Tumors. Cancer Cell 2019, 35: 204-220.e9. PMID: 30753823, PMCID: PMC7876656, DOI: 10.1016/j.ccell.2019.01.006.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsAutophagyCell Line, TumorCyclin-Dependent Kinase Inhibitor p16Endoplasmic Reticulum StressFemaleGene Expression Regulation, NeoplasticHumansMaleMice, 129 StrainMice, Inbred C57BLMice, KnockoutProteasome InhibitorsProteostasisProto-Oncogene Proteins c-mycRhabdoid TumorSignal TransductionSMARCB1 ProteinTumor Cells, CulturedTumor Suppressor Protein p53Unfolded Protein ResponseConceptsMalignant rhabdoid tumorRhabdoid tumorUnfolded protein responseClinical pathological featuresAggressive pediatric malignancyCombination of agentsPediatric malignanciesMouse modelP53 axisMosaic mouse modelChromatin remodeling genesER stress responseTumorsHuman oncogenesisBiallelic inactivationMalignancyProtein responseDramatic activationHuman diseasesMaster regulatorExquisite sensitivityAutophagic machineryAgentsDiseaseStress response
2011
Significant Biological Role of Sp1 Transactivation in Multiple Myeloma
Fulciniti M, Amin S, Nanjappa P, Rodig S, Prabhala R, Li C, Minvielle S, Tai Y, Tassone P, Avet-Loiseau H, Hideshima T, Anderson K, Munshi N. Significant Biological Role of Sp1 Transactivation in Multiple Myeloma. Clinical Cancer Research 2011, 17: 6500-6509. PMID: 21856768, PMCID: PMC4318245, DOI: 10.1158/1078-0432.ccr-11-1036.Peer-Reviewed Original ResearchConceptsBone marrow stromal cellsSp1 activitySp1 knockdownTranscription factor specificity protein 1Caspase-9-dependent apoptosisCritical cell cycleSp1 DNA bindingSp1-responsive promotersSpecificity protein 1Cell growthFirefly luciferase reporter geneImportant transcription factorImportant regulatory roleLuciferase reporter geneSignificant biological roleApoptosis-related genesSp1 transactivationShort hairpin RNASp1 DNACellular processesTranscription factorsPromoter elementsMarrow stromal cellsReporter geneMM cells