2022
Human WDR5 promotes breast cancer growth and metastasis via KMT2-independent translation regulation
Cai WL, Chen JF, Chen H, Wingrove E, Kurley SJ, Chan LH, Zhang M, Arnal-Estape A, Zhao M, Balabaki A, Li W, Yu X, Krop ED, Dou Y, Liu Y, Jin J, Westbrook TF, Nguyen DX, Yan Q. Human WDR5 promotes breast cancer growth and metastasis via KMT2-independent translation regulation. ELife 2022, 11: e78163. PMID: 36043466, PMCID: PMC9584608, DOI: 10.7554/elife.78163.Peer-Reviewed Original ResearchConceptsBreast cancer cellsMetastatic breast cancerBreast cancerRibosomal gene expressionCancer cellsKnockdown of WDR5Vivo genetic screenReversible epigenetic mechanismsGenetic screenTranslation regulationTriple-negative breast cancerEpigenetic regulatorsEpigenetic mechanismsBreast cancer growthCancer-related deathTranslation efficiencyWDR5Novel therapeutic strategiesTranslation rateGene expressionCell growthAdvanced diseaseEffective therapyMetastatic capabilityPotent suppression
2020
Specific chromatin landscapes and transcription factors couple breast cancer subtype with metastatic relapse to lung or brain
Cai WL, Greer CB, Chen JF, Arnal-Estapé A, Cao J, Yan Q, Nguyen DX. Specific chromatin landscapes and transcription factors couple breast cancer subtype with metastatic relapse to lung or brain. BMC Medical Genomics 2020, 13: 33. PMID: 32143622, PMCID: PMC7060551, DOI: 10.1186/s12920-020-0695-0.Peer-Reviewed Original ResearchConceptsOpen chromatin signaturesTranscription factorsChromatin landscapeChromosome conformation captureOpen chromatin landscapeSpecific chromatin landscapesHomophilic cell adhesionTransposase-accessible chromatinEnhancer-promoter interactionsSpecific transcription factorsActive chromatin sitesATAC-seq dataMetastatic cellsGene expression dataChromatin signaturesConformation captureChromatin sitesActive chromatinATAC-seqEpigenomic propertiesChIP-seqChromatin immunoprecipitationEndothelial cell migrationEpigenomic analysisTranscriptomic differences
2018
MSK1 regulates luminal cell differentiation and metastatic dormancy in ER+ breast cancer
Gawrzak S, Rinaldi L, Gregorio S, Arenas E, Salvador F, Urosevic J, Figueras-Puig C, Rojo F, del Barco Barrantes I, Cejalvo J, Palafox M, Guiu M, Berenguer-Llergo A, Symeonidi A, Bellmunt A, Kalafatovic D, Arnal-Estapé A, Fernández E, Müllauer B, Groeneveld R, Slobodnyuk K, Stephan-Otto Attolini C, Saura C, Arribas J, Cortes J, Rovira A, Muñoz M, Lluch A, Serra V, Albanell J, Prat A, Nebreda A, Benitah S, Gomis R. MSK1 regulates luminal cell differentiation and metastatic dormancy in ER+ breast cancer. Nature Cell Biology 2018, 20: 211-221. PMID: 29358704, DOI: 10.1038/s41556-017-0021-z.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsBiomarkers, TumorBone NeoplasmsBreast NeoplasmsCell DifferentiationChromatinFemaleGATA3 Transcription FactorGene Expression Regulation, NeoplasticGenome, HumanHepatocyte Nuclear Factor 3-alphaHumansMiceMiddle AgedNeoplasm MetastasisPrognosisReceptors, EstrogenRibosomal Protein S6 Kinases, 90-kDaRNA, Small InterferingXenograft Model Antitumor AssaysConceptsER+ breast cancerLuminal cell differentiationBreast cancerMetastatic dormancyProgression of ER+ breast cancerDifferentiation of breast cancer cellsGenome-wide short hairpin RNA screenSymptomatic bone metastasesEstrogen receptor-positiveShort hairpin RNA screenMSK1 expressionBreast cancer cellsCell differentiationFOXA1 transcription factorMetastatic latencyReceptor-positiveEarly relapseBone metastasesYears of latencyBone homingStratify patientsExpression of genesMicrometastatic lesionsImprove prognosisMetastatic progression
2015
Enhanced MAF Oncogene Expression and Breast Cancer Bone Metastasis
Pavlovic M, Arnal-Estapé A, Rojo F, Bellmunt A, Tarragona M, Guiu M, Planet E, Garcia-Albéniz X, Morales M, Urosevic J, Gawrzak S, Rovira A, Prat A, Nonell L, Lluch A, Jean-Mairet J, Coleman R, Albanell J, Gomis R. Enhanced MAF Oncogene Expression and Breast Cancer Bone Metastasis. Journal Of The National Cancer Institute 2015, 107: djv256. PMID: 26376684, PMCID: PMC4681582, DOI: 10.1093/jnci/djv256.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorBone NeoplasmsBreast NeoplasmsCell Line, TumorDNA Copy Number VariationsFemaleGene Expression Regulation, NeoplasticHeterograftsHumansImmunohistochemistryIn Situ Hybridization, FluorescenceIncidenceMiceMice, Inbred BALB COdds RatioPredictive Value of TestsPrognosisProportional Hazards ModelsProto-Oncogene Proteins c-mafUp-RegulationConceptsBreast cancer bone metastasisCopy number aberrationsCancer bone metastasisBone metastasesRisk of bone metastasisAssociated with bone metastasisBreast cancer cells in vivoPrimary breast tumorsBreast cancer patient populationCancer cells in vivoMetastasis to boneClinical follow-upBreast cancer cellsAssociated with riskCells in vivoCancer patient populationBone relapseCause-specific hazard modelBreast tumorsFollow-upMAF overexpressionMetastasisPatient populationProtein overexpressionCancer cells
2012
Identification of NOG as a Specific Breast Cancer Bone Metastasis-supporting Gene* ♦
Tarragona M, Pavlovic M, Arnal-Estapé A, Urosevic J, Morales M, Guiu M, Planet E, González-Suárez E, Gomis R. Identification of NOG as a Specific Breast Cancer Bone Metastasis-supporting Gene* ♦. Journal Of Biological Chemistry 2012, 287: 21346-21355. PMID: 22547073, PMCID: PMC3375555, DOI: 10.1074/jbc.m112.355834.Peer-Reviewed Original ResearchConceptsBreast cancer cellsCancer cellsPrimary siteNOG expressionBone metastatic potentialBone metastatic lesionsMetastatic breast cancer cellsHuman breast cancer cellsAggressive cancer cellsBone relapseMetastatic lesionsPrimary tumorMetastatic nicheTumor cellsBone colonizationMetastatic potentialDistant organsMetastasisOsteoclast differentiationColonic functionBone degradationCell functionNOGBMP inhibitorsBone
2011
Tumor-stroma interactions a trademark for metastasis
Morales M, Planet E, Arnal-Estape A, Pavlovic M, Tarragona M, Gomis R. Tumor-stroma interactions a trademark for metastasis. The Breast 2011, 20: s50-s55. PMID: 22015293, DOI: 10.1016/s0960-9776(11)70294-6.Peer-Reviewed Original ResearchConceptsGenes associated with metastasisTumor-stroma interactionsPrimary tumorRisk of relapseTumor-stroma communicationAssociated with metastasisDisseminated diseaseMetastatic nestsMetastatic developmentImmune infiltrationBone colonizationClinical correlatesSystemic instigationMetastasisTumorCytokine-cytokine receptor interactionReceptor interactionCytokine-cytokine receptor interaction pathwayExpression profiling dataGenesRelapseLungPathway
2010
HER2 Silences Tumor Suppression in Breast Cancer Cells by Switching Expression of C/EBPβ Isoforms
Arnal-Estapé A, Tarragona M, Morales M, Guiu M, Nadal C, Massagué J, Gomis R. HER2 Silences Tumor Suppression in Breast Cancer Cells by Switching Expression of C/EBPβ Isoforms. Cancer Research 2010, 70: 9927-9936. PMID: 21098707, DOI: 10.1158/0008-5472.can-10-0869.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsBlotting, WesternBreast NeoplasmsCCAAT-Enhancer-Binding Protein-betaCell LineCell Line, TumorCellular SenescenceGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, FluorescenceMiceMice, NudePhosphorylationPromoter Regions, GeneticProtein BindingProtein BiosynthesisProtein IsoformsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycReceptor, ErbB-2Reverse Transcriptase Polymerase Chain ReactionRNA InterferenceTransforming Growth Factor betaTrastuzumabConceptsBreast cancer cellsTumor suppressionBreast cancerOncogene-induced senescenceCancer cellsHER2-overexpressing breast cancer cellsSubtypes of breast cancerHER2 antibody trastuzumabTransforming growth factor-bBreast cancer developmentGrowth factor BTranscriptional repressor complexHER2 signalingSuppressor responseTumor progressionMammary epithelial cellsAntibody trastuzumabHER2Cancer developmentEpithelial cellsSuppressor functionSwitching expressionInterfere with activitiesMYC promoterBreast