2024
Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment
Martinez-Terroba E, Plasek-Hegde L, Chiotakakos I, Li V, de Miguel F, Robles-Oteiza C, Tyagi A, Politi K, Zamudio J, Dimitrova N. Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment. Science Immunology 2024, 9: eadh5462. PMID: 38875320, DOI: 10.1126/sciimmunol.adh5462.Peer-Reviewed Original ResearchConceptsTumor microenvironmentLung adenocarcinomaMetastatic diseasePromoting metastatic diseaseGlobal chromatin accessibilityMetastasis-associated lung adenocarcinoma transcript 1Overexpression of MALAT1Lung adenocarcinoma transcript 1Lung adenocarcinoma metastasisCCL2 blockadeInflammatory reprogrammingEnhanced cell mobilityMacrophage depletionMechanism of actionTumor typesTumor progressionMouse modelCell mobilizationTumorLong noncoding RNAsParacrine secretionMetastasisCell linesTranscript 1Microenvironment
2021
The p53 transcriptional response across tumor types reveals core and senescence-specific signatures modulated by long noncoding RNAs
Tesfaye E, Martinez-Terroba E, Bendor J, Winkler L, Olivero C, Chen K, Feldser DM, Zamudio JR, Dimitrova N. The p53 transcriptional response across tumor types reveals core and senescence-specific signatures modulated by long noncoding RNAs. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2025539118. PMID: 34326251, PMCID: PMC8346867, DOI: 10.1073/pnas.2025539118.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinogenesisCell Line, TumorCell ProliferationCellular SenescenceDNA DamageE2F Transcription FactorsGene Expression Regulation, NeoplasticGenome-Wide Association StudyMiceNeoplasmsProto-Oncogene Proteins c-mycRNA, Long NoncodingSignal TransductionStress, PhysiologicalTumor Suppressor Protein p53ConceptsOncogenic contextPermanent cell cycle arrestP53-induced lncRNAsP53 transcriptional responseMYC target genesTumor suppressor mechanismRepression of E2FP53-binding siteP53-dependent senescenceTumor-type specificCell cycle arrestTranscriptional responseProliferative arrestTarget genesMurine cancer cell linesTranscriptional signatureRegulatory axisTumor typesCycle arrestP53 functionDistinct tumor typesFunctional investigationDownstream mediatorP53 pathwayCancer cell lines
2016
Stromal Expression of miR-143/145 Promotes Neoangiogenesis in Lung Cancer Development
Dimitrova N, Gocheva V, Bhutkar A, Resnick R, Jong RM, Miller KM, Bendor J, Jacks T. Stromal Expression of miR-143/145 Promotes Neoangiogenesis in Lung Cancer Development. Cancer Discovery 2016, 6: 188-201. PMID: 26586766, PMCID: PMC4744583, DOI: 10.1158/2159-8290.cd-15-0854.Peer-Reviewed Original Research