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
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 inhibitorsBoneEpithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cells
Celià-Terrassa T, Meca-Cortés Ó, Mateo F, de Paz A, Rubio N, Arnal-Estapé A, Ell B, Bermudo R, Díaz A, Guerra-Rebollo M, Lozano J, Estarás C, Ulloa C, ρlvarez-Simón D, Milà J, Vilella R, Paciucci R, Martínez-Balbás M, de Herreros A, Gomis R, Kang Y, Blanco J, Fernández P, Thomson T. Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cells. Journal Of Clinical Investigation 2012, 122: 1849-1868. PMID: 22505459, PMCID: PMC3366719, DOI: 10.1172/jci59218.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, DifferentiationCadherinsCell Line, TumorCell MovementCell ShapeCoculture TechniquesEpithelial CellsEpithelial-Mesenchymal TransitionGene Expression ProfilingGene Regulatory NetworksHomeodomain ProteinsHumansMaleMiceMice, Inbred NODMice, SCIDNeoplasm InvasivenessNeoplasm MetastasisNeoplasm StagingNeoplasm TransplantationProstatic NeoplasmsRepressor ProteinsSnail Family Transcription FactorsSpheroids, CellularTranscription FactorsTwist-Related Protein 1Urinary Bladder NeoplasmsZinc Finger E-box-Binding Homeobox 1ConceptsEpithelial-mesenchymal transitionDistant metastasisSelf-renewalGene programTumor-initiating cellsEpithelial-mesenchymal transition programProstate cancer cellsIn vitro invasionPrimary implantation sitesHuman cellular modelsMetastatic populationBladder cancerTumor subpopulationsLocal invasionMesenchymal-likeEpithelial featuresMetastatic phenotypeNeoplastic cellsMalignant progressionImplantation sitesMesenchymal traitsEMT factorsCancer cellsMesenchymal genesIn vivo
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