2020
Tumor progression and chromatin landscape of lung cancer are regulated by the lineage factor GATA6
Arnal-Estapé A, Cai WL, Albert AE, Zhao M, Stevens LE, López-Giráldez F, Patel KD, Tyagi S, Schmitt EM, Westbrook TF, Nguyen DX. Tumor progression and chromatin landscape of lung cancer are regulated by the lineage factor GATA6. Oncogene 2020, 39: 3726-3737. PMID: 32157212, PMCID: PMC7190573, DOI: 10.1038/s41388-020-1246-z.Peer-Reviewed Original ResearchConceptsChromatin landscapeTranscription factorsBone morphogenetic protein (BMP) signalingDiverse transcriptional programsAlters chromatin accessibilityMultiple genomic lociMorphogenetic protein signalingDistal enhancer elementsSelective transcription factorsEpithelial cell typesSurfactant protein CChromatin accessibilityGenomic lociTranscriptional programsLung adenocarcinoma progressionTumor progressionEpigenetic mechanismsProtein signalingBiological functionsLUAD progressionLUAD cellsEnhancer elementsLineage dependencyTumor suppressionLung cancer cells
2019
Adaptive Protein Translation by the Integrated Stress Response Maintains the Proliferative and Migratory Capacity of Lung Adenocarcinoma Cells
Albert AE, Adua SJ, Cai WL, Arnal-Estapé A, Cline GW, Liu Z, Zhao M, Cao PD, Mariappan M, Nguyen DX. Adaptive Protein Translation by the Integrated Stress Response Maintains the Proliferative and Migratory Capacity of Lung Adenocarcinoma Cells. Molecular Cancer Research 2019, 17: 2343-2355. PMID: 31551255, PMCID: PMC6938689, DOI: 10.1158/1541-7786.mcr-19-0245.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 4Adenocarcinoma of LungAmino AcidsCarbon-Nitrogen Ligases with Glutamine as Amide-N-DonorCell Line, TumorCell ProliferationCyclin B1Eukaryotic Initiation Factor-2Gene Expression Regulation, NeoplasticHumansNF-E2-Related Factor 2Oxidative StressPhosphatidylinositol 3-KinasesProtein BiosynthesisProteostasisSignal TransductionStress, PhysiologicalTOR Serine-Threonine KinasesConceptsIntegrated stress responseProtein translationCell cycle progressionLung adenocarcinoma cellsLung cancer cellsNew regulatory layerCertain oncogenic mutationsAmino acid limitationNovel regulatory mechanismControl of proteostasisCancer cellsDifferent biological consequencesEIF2α-dependent mannerAmino acid metabolismAdenocarcinoma cellsNrf2 protein levelsPI3K pathwayConserved pathwayRegulatory layerISR pathwayATF4 branchCell cycle regulator cyclin B1MTOR/PI3K pathwaySelect proteinsAsparagine synthetase
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 ResearchMeSH KeywordsBone NeoplasmsBreast NeoplasmsCarrier ProteinsCell DifferentiationCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansNeoplasm MetastasisOrgan SpecificityOsteoclastsConceptsBreast 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 ResearchMeSH KeywordsBiomarkers, TumorBreast NeoplasmsCell CommunicationCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleNeoplasm MetastasisReceptors, CytokineSampling StudiesSensitivity and SpecificityStromal CellsConceptsGenes 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