0000000000740650

AUTHOR

Micaela Montanari

showing 3 related works from this author

CTCF and BORIS Regulate Rb2/p130 Gene Transcription: A Novel Mechanism and a New Paradigm for Understanding the Biology of Lung Cancer

2011

Abstract Although innumerable investigations regarding the biology of lung cancer have been carried out, many aspects thereof remain to be addressed, including the role played by the retinoblastoma-related protein Rb2/p130 during the evolution of this disease. Here we report novel findings on the mechanisms that control Rb2/p130 gene expression in lung fibroblasts and characterize the effects of Rb2/p130 deregulation on the proliferative features of lung cancer cells. We revealed for the first time that in lung fibroblasts the expression of Rb2/p130 gene is directly controlled by the chromatin insulator CCCTC-binding factor, CTCF, which by binding to the Rb2/p130 gene promoter induces, and/…

CCCTC-Binding FactorChromatin ImmunoprecipitationCancer ResearchLung NeoplasmsTranscription GeneticSettore MED/06 - Oncologia MedicaBiologyInsulator (genetics)Open Reading FramesTranscription (biology)Carcinoma Non-Small-Cell LungCell Line TumorGene expressionmedicineHumansCarcinoma Small CellPromoter Regions GeneticLung cancerChromosome PositioningMolecular BiologyGeneBinding SitesRetinoblastoma-Like Protein p130PromoterFibroblastsmedicine.diseaseChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsGene transcriptionOncologyCTCFembryonic structuresCancer researchLung cancerLung cancer; Gene transcriptionbiological phenomena cell phenomena and immunityProtein BindingMolecular Cancer Research
researchProduct

Nuclear and cytoplasmic interaction of pRb2/p130 and ER-β in MCF-7 breast cancer cells

2006

Estrogens exhibit important biological functions and influence several pathological processes of hormone-dependent diseases. The biological actions of estrogens require their interaction with two estrogen receptors (ER-alpha and ER-beta), which are ligand-dependent transcription factors. ER-alpha and ER-beta exhibit distinct tissue expression patterns as well as show different patterns of gene regulation. In addition, it has been suggested that ER-beta works as a counter partner of ER-alpha through inhibition of the transactivating functions of ER-alpha. For instance, ER-beta seems to play a different role in breast tumorigenesis than ER-alpha, as ER-beta decreased expression in breast canc…

OncologyCytoplasmmedicine.medical_specialtyMolecular Sequence DataEstrogen receptorBreast NeoplasmsEstrogen receptorsmedicine.disease_causeBreast cancerBreast cancerCancer stem cellCell Line TumorInternal medicinemedicineEstrogen Receptor betaHumansImmunoprecipitationGene silencingAmino Acid SequenceTranscription factorBreast cancer; Estrogen receptors; Estrogens; pRb2/130Cell NucleusRegulation of gene expressionRetinoblastoma-Like Protein p130business.industryEstrogensHematologymedicine.diseaseOncologyMCF-7Cancer researchbusinessCarcinogenesispRb2/130
researchProduct

Modulation of Cell Cycle Components by Epigenetic and Genetic Events

2005

Cell cycle progression is monitored by surveillance mechanisms, or cell cycle checkpoints, that ensure that initiation of a later event is coupled with the completion of an early cell cycle event. Deregulated proliferation is a characteristic feature of tumor cells. Moreover, defects in many of the molecules that regulate the cell cycle have been implicated in cancer formation and progression. Key among these are p53, the retinoblastoma protein (pRb) and its related proteins, p107 and pRb2/p130, and cdk inhibitors (p15, p16, p18, p19, p21, p27), all of which act to keep the cell cycle from progressing until all repairs to damaged DNA have been completed. The pRb (pRb/p16(INK4a)/cyclin D1) a…

Cell cycle checkpointCyclin ABiologymedicine.disease_causeModels BiologicalRetinoblastoma ProteinEpigenesis GeneticCyclin-dependent kinaseNeoplasmsmedicineAnimalsHumansEpigeneticsCell ProliferationCell growthCell CycleRetinoblastoma proteinHematologyCell cycleCell biologyOncologyDisease Progressionbiology.proteinTumor Suppressor Protein p53biological phenomena cell phenomena and immunityCarcinogenesisSignal TransductionSeminars in Oncology
researchProduct