Search results for "Tumor Protein p73"

showing 3 items of 3 documents

ΔNp73β is oncogenic in hepatocellular carcinoma by blocking apoptosis signaling via death receptors and mitochondria

2010

p73 belongs to the p53 family of transcription factors known to regulate cell cycle and apoptosis. The Trp73 gene has two promoters that drive the expression of two major p73 isoform subfamilies: TA and ΔN. In general, TAp73 isoforms show proapoptotic activities, whereas members of the N-terminally truncated (ΔN) p73 subfamily that lack the transactivation domain show antiapoptotic functions. We found that upregulation of ΔNp73 in hepatocellular carcinoma (HCC) correlated with reduced survival. Here, we investigated the molecular mechanisms accounting for the oncogenic role of ΔNp73 in HCC.ΔNp73β can directly interfere with the transcriptional activation function of the TA (containing the t…

Gene isoformCarcinoma HepatocellularMolecular Sequence DataApoptosisBiologyModels BiologicalTransactivationDownregulation and upregulationCell Line TumorHumansProtein IsoformsMolecular BiologyTranscription factorGenes DominantOligonucleotide Array Sequence Analysisbcl-2-Associated X ProteinRegulation of gene expressionBase SequenceSettore BIO/11Gene Expression ProfilingTumor Suppressor ProteinsLiver NeoplasmsNuclear ProteinsTumor Protein p73PromoterReceptors Death DomainCell BiologyCell cyclePrognosisMitochondriaCell biologyDNA-Binding ProteinsEnzyme ActivationGene Expression Regulation NeoplasticDrug Resistance NeoplasmCaspasesCancer researchTumor Suppressor Protein p53Signal transductionPrecancerous ConditionsSignal TransductionDevelopmental BiologyCell Cycle
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The NUPR1/p73 axis contributes to sorafenib resistance in hepatocellular carcinoma

2021

The multikinase inhibitor sorafenib was the first drug approved by the FDA for treating patients with advanced hepatocellular carcinoma (HCC). However, sorafenib resistance remains a major challenge for improving the effectiveness of HCC treatment. Previously, we identified several genes modulated after sorafenib treatment of human HCC cells, including the stress-inducible nuclear protein 1 (NUPR1) gene. Multiple studies have shown that NUPR1 regulates autophagy, apoptosis, and chemoresistance. Here, we demonstrate that treatment of HCC cells with sorafenib resulted in the activation of autophagic flux. NUPR1 knock-down (KD) in HCC cells was associated with increased p62 expression, suggest…

SorafenibCancer ResearchCarcinoma HepatocellularSettore MED/09 - Medicina InternaHepatocellular carcinomap73Mice NudeApoptosisSettore BIO/11 - Biologia MolecolareMiceNSC5594In vivoPumaBasic Helix-Loop-Helix Transcription FactorsmedicineAutophagyNSC5994AnimalsHumansGene silencingneoplasmsbiologyActivator (genetics)business.industryLiver NeoplasmsAutophagyApoptosiTumor Protein p73Hep G2 CellsSorafenibbiology.organism_classificationmedicine.diseasedigestive system diseasesNeoplasm ProteinsOncologyDrug Resistance NeoplasmApoptosisHepatocellular carcinomaCancer researchFemalebusinessNUPR1medicine.drug
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p73 deficiency results in impaired self renewal and premature neuronal differentiation of mouse neural progenitors independently of p53

2010

10 p.-5 fig.

p53Cancer ResearchGenotypeCellular differentiationImmunologyPopulationp73RegulatorBiologyCellular and Molecular NeuroscienceMiceNeurosphereAnimalsProgenitor celleducationCell ProliferationNeuronsNeural stem cellseducation.field_of_studyCell growthTumor Suppressor ProteinsNuclear ProteinsCell DifferentiationNeurodegenerative DiseasesTumor Protein p73Cell BiologyEmbryonic stem cellasymmetric divisionNeural stem cellCell biologyDNA-Binding ProteinsDifferentiationSelf-renewalOriginal ArticleTumor Suppressor Protein p53
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