2024
CRISPR-based dissection of microRNA-23a ~ 27a ~ 24-2 cluster functionality in hepatocellular carcinoma
Cui M, Liu Z, Wang S, Bae S, Guo H, Zhou J, Liu R, Wang L. CRISPR-based dissection of microRNA-23a ~ 27a ~ 24-2 cluster functionality in hepatocellular carcinoma. Oncogene 2024, 43: 2708-2721. PMID: 39112518, PMCID: PMC11364504, DOI: 10.1038/s41388-024-03115-z.Peer-Reviewed Original ResearchConceptsMiR-23aMiR-27aCRISPR interferenceCRISPR activationHigh-throughput RNA-seqCell migrationCDK1/cyclin B activityReduced cell growth in vitroMiRNA target predictionCell cycle arrestMiRNA clusterHepatocellular carcinoma cellsCell growth in vitroRNA-seqGene networksTarget predictionCRISPR knockoutOncogenic roleGrowth in vitroCycle arrestMature miRNAsMiRNAsG2/M phaseSignaling pathwayOncogenic function
2023
Design of Class I/IV Bromodomain-Targeting Degraders for Chromatin Remodeling Complexes
Zahid H, Costello J, Li Y, Kimbrough J, Actis M, Rankovic Z, Yan Q, Pomerantz W. Design of Class I/IV Bromodomain-Targeting Degraders for Chromatin Remodeling Complexes. ACS Chemical Biology 2023, 18: 1278-1293. PMID: 37260298, PMCID: PMC10698694, DOI: 10.1021/acschembio.2c00902.Peer-Reviewed Original ResearchConceptsChromatin Remodeling ComplexNon-BET bromodomainsRemodeling complexProtein degradationHeterobifunctional moleculesBET familyProtein targetsPyrimidine base analogsNumber of degradersDegradersOncogenic roleTernary complexExit vectorsWestern blottingProteinFirst exampleClass IChallenging targetComplexesCECR2ChromatinBromodomainsBPTFFamilyNanoBRETPhosphorylation stabilized TET1 acts as an oncoprotein and therapeutic target in B cell acute lymphoblastic leukemia
Chen Z, Zhou K, Xue J, Small A, Xiao G, Nguyen L, Zhang Z, Prince E, Weng H, Huang H, Zhao Z, Qing Y, Shen C, Li W, Han L, Tan B, Su R, Qin H, Li Y, Wu D, Gu Z, Ngo V, He X, Chao J, Leung K, Wang K, Dong L, Qin X, Cai Z, Sheng Y, Chen Y, Wu X, Zhang B, Shi Y, Marcucci G, Qian Z, Xu M, Müschen M, Chen J, Deng X. Phosphorylation stabilized TET1 acts as an oncoprotein and therapeutic target in B cell acute lymphoblastic leukemia. Science Translational Medicine 2023, 15: eabq8513. PMID: 36989375, PMCID: PMC11163962, DOI: 10.1126/scitranslmed.abq8513.Peer-Reviewed Original ResearchConceptsB-cell acute lymphoblastic leukemiaCell acute lymphoblastic leukemiaAcute lymphoblastic leukemiaB-ALLRefractory/Oncogenic roleLymphoblastic leukemiaProtein kinase C epsilonOverall survival rateNormal precursor B cellsCrucial oncogenic rolePrecursor B cellsAdult patientsPDX modelsPharmacological targetingTherapeutic targetB cellsImproved therapiesSurvival rateLeukemia progressionTherapeutic potentialOverexpression of TET1TET1 proteinATM serine/threonine kinaseLeukemia
2022
Epigenetic regulation of EIF4A1 through DNA methylation and an oncogenic role of eIF4A1 through BRD2 signaling in prostate cancer
Wang C, Leavenworth J, Zhang C, Liu Z, Yuan K, Wang Y, Zhang G, Wang S, Cui X, Zhang Y, Bae S, Zhou J, Wang L, Liu R. Epigenetic regulation of EIF4A1 through DNA methylation and an oncogenic role of eIF4A1 through BRD2 signaling in prostate cancer. Oncogene 2022, 41: 2778-2785. PMID: 35361883, PMCID: PMC9215223, DOI: 10.1038/s41388-022-02272-3.Peer-Reviewed Original ResearchConceptsCpG-rich islandDNA methylationProstate cancer cellsEpigenetic regulationPrimary prostate cancerProstate cancerTargets of DNA methylationCancer cellsCRISPR-Cas9-based toolHuman prostate cancer cellsOncogenic roleCancer cell proliferation in vitroProstate cancer in vitroTranslational regulationOncogenic translationProtein translationUntranslated regionTumor growth in vivoNormal prostate tissueRNA sequencingCell proliferation in vitroCancer in vitroEIF4A1Growth in vivoElevated mRNA levels
2019
Identification of ZNF217 As an Essential Oncogenic Gene in B-Cell Acute Lymphoblastic Leukemia By CRISPR/Cas9-Based Library Screening
Qin X, Su R, Yang L, Chan A, Deng X, Qing Y, Klemm L, Müschen M, Chen C, Chen J. Identification of ZNF217 As an Essential Oncogenic Gene in B-Cell Acute Lymphoblastic Leukemia By CRISPR/Cas9-Based Library Screening. Blood 2019, 134: 1465. DOI: 10.1182/blood-2019-129849.Peer-Reviewed Original ResearchB-cell acute lymphoblastic leukemiaBCR-ABL1 fusionAcute lymphoblastic leukemiaAcute myeloid leukemiaAML cellsM6A regulatorsMLL-AF4 fusionAdult patientsLymphoblastic leukemiaPediatric B-cell acute lymphoblastic leukemiaEssential oncogenic roleM6A modificationMessenger RNACytogenetic characteristicsDismal survivalMyeloid leukemiaB cell progenitorsTherapeutic targetOncogenic roleSolid tumorsPatientsZinc finger protein 217B-lineageLeukemiaCytogenetic changesPPM1D mutations silence NAPRT gene expression and confer NAMPT inhibitor sensitivity in glioma
Fons NR, Sundaram RK, Breuer GA, Peng S, McLean RL, Kalathil AN, Schmidt MS, Carvalho DM, Mackay A, Jones C, Carcaboso ÁM, Nazarian J, Berens ME, Brenner C, Bindra RS. PPM1D mutations silence NAPRT gene expression and confer NAMPT inhibitor sensitivity in glioma. Nature Communications 2019, 10: 3790. PMID: 31439867, PMCID: PMC6706443, DOI: 10.1038/s41467-019-11732-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsBrain Stem NeoplasmsCell Line, TumorChildCytokinesDiffuse Intrinsic Pontine GliomaDNA MethylationEpigenetic RepressionFemaleGene Expression Regulation, NeoplasticHumansMiceNicotinamide PhosphoribosyltransferasePonsPrimary Cell CultureProtein Phosphatase 2CSynthetic Lethal MutationsXenograft Model Antitumor AssaysConceptsNicotinic acid phosphoribosyltransferaseSynthetic lethal interactionsNAMPT inhibitorsTumor-specific cell killingProtein phosphataseEpigenetic silencingMutant cellsKey genesCpG islandsLethal interactionsNAD biosynthesisGene expressionInhibitor sensitivityNAD metabolismOncogenic rolePediatric gliomasMutationsModel systemCell killingDriver mutationsPediatric high-grade gliomasMutant tumorsOncogenic driver mutationsNicotinamide phosphoribosyltransferase (NAMPT) inhibitionGenome
2017
MicroRNAs of the mir-17~92 cluster regulate multiple aspects of pancreatic tumor development and progression
Quattrochi B, Gulvady A, Driscoll D, Sano M, Klimstra D, Turner C, Lewis B. MicroRNAs of the mir-17~92 cluster regulate multiple aspects of pancreatic tumor development and progression. Oncotarget 2017, 5: 35902-35918. PMID: 28415794, PMCID: PMC5482626, DOI: 10.18632/oncotarget.16277.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAllelesAnimalsCarcinoma, Intraductal, NoninfiltratingCarcinoma, Pancreatic DuctalCell Line, TumorCell Transformation, NeoplasticDisease ProgressionGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockout TechniquesHumansMAP Kinase Signaling SystemMiceMice, TransgenicMicroRNAsMultigene FamilyNeoplasm InvasivenessPancreatic NeoplasmsPhenotypeConceptsMiR-17~92MiR-19MiR-17~92 clusterCluster of microRNAsTranswell assayMiRNAsOncogenic roleMicroRNAsCell invasionPromote cancer cell invasionAntagomirCell linesCancer cell invasionERK pathway activationPancreatic ductal adenocarcinomaMaintenance in vivoStages of pancreatic tumorigenesisPrecursorPancreatic tumor development
2015
NFATc1 promotes prostate tumorigenesis and overcomes PTEN loss-induced senescence
Manda K, Tripathi P, Hsi A, Ning J, Ruzinova M, Liapis H, Bailey M, Zhang H, Maher C, Humphrey P, Andriole G, Ding L, You Z, Chen F. NFATc1 promotes prostate tumorigenesis and overcomes PTEN loss-induced senescence. Oncogene 2015, 35: 3282-3292. PMID: 26477312, PMCID: PMC5012433, DOI: 10.1038/onc.2015.389.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell LineCell Line, TumorCell ProliferationCell Transformation, NeoplasticCellular SenescenceCytokinesGene Expression Regulation, NeoplasticHumansImmunohistochemistryMaleMice, KnockoutMice, NudeMice, TransgenicNFATC Transcription FactorsProstateProstatic NeoplasmsPTEN PhosphohydrolaseReverse Transcriptase Polymerase Chain ReactionTransplantation, HomologousTumor Cells, CulturedTumor MicroenvironmentConceptsProstate tumorigenesisHuman PCaNFATc1 activationNon-tumorigenic prostate cellsActivated T cells c1Cultured PCa cellsT cells c1Cellular senescenceRole of NFATc1Number of cytokinesActivation of NFATc1Proinflammatory cytokinesPCa cellsProstate cancerProstatic adenocarcinomaLuminal epitheliumMouse prostateCells c1Normal prostateOncogenic roleOncogene c-mycProstate tissueProstate cellsSoluble factorsNuclear factor
2014
CSF1-ETS2-induced microRNA in myeloid cells promote metastatic tumor growth
Mathsyaraja H, Thies K, Taffany D, Deighan C, Liu T, Yu L, Fernandez S, Shapiro C, Otero J, Timmers C, Lustberg M, Chalmers J, Leone G, Ostrowski M. CSF1-ETS2-induced microRNA in myeloid cells promote metastatic tumor growth. Oncogene 2014, 34: 3651-3661. PMID: 25241894, PMCID: PMC4369473, DOI: 10.1038/onc.2014.294.Peer-Reviewed Original ResearchConceptsTumor-infiltrating myeloid cellsMetastatic tumor growthMyeloid cellsMiR-21Breast cancerTumor growthHuman metastatic breast cancerMetastatic tumor burdenMetastatic breast cancerPro-tumor functionsAnti-angiogenic genesAttractive therapeutic targetTumor cell proliferationPro-angiogenic propertiesMature myeloid cellsTumor burdenMonocytes correlatesPoor prognosisMelanoma metastasesMouse modelTherapeutic targetSolid tumorsOncogenic roleSurvival rateTherapeutic efficacy
2013
Paradoxical role of the proto-oncogene Axl and Mer receptor tyrosine kinases in colon cancer
Bosurgi L, Bernink JH, Cuevas V, Gagliani N, Joannas L, Schmid ET, Booth CJ, Ghosh S, Rothlin CV. Paradoxical role of the proto-oncogene Axl and Mer receptor tyrosine kinases in colon cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 13091-13096. PMID: 23878224, PMCID: PMC3740859, DOI: 10.1073/pnas.1302507110.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAxl Receptor Tyrosine KinaseAzoxymethanec-Mer Tyrosine KinaseColitisColonColonic NeoplasmsCytokinesDextran SulfateFemaleFlow CytometryGene ExpressionMacrophagesMaleMiceMice, Inbred StrainsMice, KnockoutMucous MembraneNeutrophilsPhagocytosisProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReverse Transcriptase Polymerase Chain ReactionSignal TransductionConceptsTumor-promoting environmentMer receptor tyrosine kinaseSystemic anticancer therapyDextran sulfate sodiumAnticancer therapyIntestinal lamina propriaAnti-inflammatory functionsInflammation-associated cancerPotential adverse effectsInflammatory signatureDendritic cellsSulfate sodiumIntestinal macrophagesProinflammatory cytokinesLamina propriaColon cancerTherapeutic targetingOncogenic roleMer inhibitorsApoptotic neutrophilsAxlMultiple cancer hallmarksReceptor tyrosine kinasesTumor cellsAdverse effects
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
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