Search results for "Tumor Suppressor Proteins"

showing 10 items of 123 documents

Low density lipoprotein receptor-related protein 1 mediated endocytosis of β1-integrin influences cell adhesion and cell migration.

2015

The low density lipoprotein receptor-related protein 1 (LRP1) has been shown to interact with β1-integrin and regulate its surface expression. LRP1 knock-out cells exhibit altered cytoskeleton organization and decreased cell migration. Here we demonstrate coupled endocytosis of LRP1 and β1-integrin and the involvement of the intracellular NPxY2 motif of LRP1 in this process. Mouse embryonic fibroblasts harboring a knock in replacement of the NPxY2 motif of LRP1 by a multiple alanine cassette (AAxA) showed elevated surface expression of β1-integrin and decreased β1-integrin internalization rates. As a consequence, cell spreading was altered and adhesion rates were increased in our cell model…

0301 basic medicineIntegrinBiologyFocal adhesion03 medical and health sciencesMiceCell MovementCell AdhesionAnimalsCell adhesionMice KnockoutCell adhesion moleculeIntegrin beta1Tumor Suppressor ProteinsCell migrationCell BiologyLRP1EndocytosisCell biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyReceptors LDLbiology.proteinNeural cell adhesion moleculeIntracellularLow Density Lipoprotein Receptor-Related Protein-1Experimental cell research
researchProduct

Novel Approaches for Glioblastoma Treatment: Focus on Tumor Heterogeneity, Treatment Resistance, and Computational Tools

2019

BACKGROUND: Glioblastoma (GBM) is a highly aggressive primary brain tumor. Currently, the suggested line of action is the surgical resection followed by radiotherapy and treatment with the adjuvant temozolomide (TMZ), a DNA alkylating agent. However, the ability of tumor cells to deeply infiltrate the surrounding tissue makes complete resection quite impossible, and in consequence, the probability of tumor recurrence is high, and the prognosis is not positive. GBM is highly heterogeneous and adapts to treatment in most individuals. Nevertheless, these mechanisms of adaption are unknown. RECENT FINDINGS: In this review, we will discuss the recent discoveries in molecular and cellular heterog…

Cancer Researchmedicine.medical_treatmentDNA Mutational AnalysisBrain tumorBioinformaticsComplete resectionTumor heterogeneityCancer VaccinesMicrotubulesArticleClonal EvolutionMachine LearningGenetic HeterogeneityCancer stem cellAntineoplastic Combined Chemotherapy ProtocolsTumor MicroenvironmentMedicineHumansTreatment resistancePrecision MedicineDNA Modification MethylasesImmune Checkpoint InhibitorsTemozolomideModels Geneticbusiness.industryBrain NeoplasmsTumor Suppressor ProteinsBrainComputational BiologyChemoradiotherapy Adjuvantmedicine.diseasePrognosisRadiation therapyDNA Repair EnzymesOncologyDrug Resistance NeoplasmMutationTumor Suppressor Protein p53businessGlioblastomaGlioblastomamedicine.drug
researchProduct

Translational readthrough of ciliopathy genes BBS2 and ALMS1 restores protein, ciliogenesis and function in patient fibroblasts

2021

Abstract Background Ciliary dysfunction underlies a range of genetic disorders collectively termed ciliopathies, for which there are no treatments available. Bardet-Biedl syndrome (BBS) is characterised by multisystemic involvement, including rod-cone dystrophy and renal abnormalities. Together with Alstrom syndrome (AS), they are known as the ‘obesity ciliopathies’ due to their common phenotype. Nonsense mutations are responsible for approximately 11% and 40% of BBS and AS cases, respectively. Translational readthrough inducing drugs (TRIDs) can restore full-length protein bypassing in-frame premature termination codons, and are a potential therapeutic approach for nonsense-mediated ciliop…

BBS2AdultMaleMedicine (General)AdolescentNonsense mutationAminopyridinesCell Cycle ProteinsCiliopathiesGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundR5-920AtalurenCiliogenesismedicineHumansReceptors SomatostatinBardet-Biedl SyndromeAlstrom SyndromeCells CulturedOxadiazolesbusiness.industryTumor Suppressor ProteinsTranslational readthroughRProteinsGeneral MedicineFibroblastsmedicine.diseaseNonsense suppressionCiliopathiesAtalurenCiliopathyALMS1chemistryCodon NonsenseAmlexanoxCancer researchMedicineBBS2businessAlström syndromeResearch PaperEBioMedicine
researchProduct

Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
researchProduct

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
researchProduct

Influence of DNA Repair on Nonlinear Dose-Responses for Mutation

2013

Recent evidence has challenged the default assumption that all DNA-reactive alkylating agents exhibit a linear dose-response. Emerging evidence suggests that the model alkylating agents methyl- and ethylmethanesulfonate and methylnitrosourea (MNU) and ethylnitrosourea observe a nonlinear dose-response with a no observed genotoxic effect level (NOGEL). Follow-up mechanistic studies are essential to understand the mechanism of cellular tolerance and biological relevance of such NOGELs. MNU is one of the most mutagenic simple alkylators. Therefore, understanding the mechanism of mutation induction, following low-dose MNU treatment, sets precedence for weaker mutagenic alkylating agents. Here, …

Hypoxanthine PhosphoribosyltransferaseMethyltransferaseDNA RepairDNA repairBiologyToxicologymedicine.disease_causePolymerase Chain ReactionCell Linechemistry.chemical_compoundalkylating agentsmedicineHumansnon-linearDNA Modification Methylasesgenetic toxicologyHypoxanthineDNA Primersdose-responsemutagenBase SequenceDose-Response Relationship DrugTumor Suppressor ProteinsgenotoxicityMutagenesisrisk assessmentDNA adductsO-6-methylguanine-DNA methyltransferaseMolecular biologyDNA Repair EnzymeschemistryMutationNOGELGenotoxicityMutagensResearch ArticleHypoxanthine PhosphoribosyltransferaseEthylnitrosoureaToxicological Sciences
researchProduct

PML as a potential predictive factor of oxaliplatin/fluoropyrimidine-based first line chemotherapy efficacy in colorectal cancer patients

2012

PML regulates a wide range of pathways involved in tumorigenesis, such as apoptosis, which is also one of the main mechanisms through which oxaliplatin and fluoropyrimidine exert their antineoplastic activity. The present study aims to investigate PML expression as a predictive factor of oxaliplatin/fluoropyrimidine therapy efficacy. Seventy-four metastatic colorectal cancer patients who received oxaliplatin/floropyrimidine-based first line therapy have been included in this retrospective study. PML expression was assessed by immunohistochemistry. PML down-regulation was detected in 39 (52.7%) patients (14 complete and 25 partial PML loss). RR was significantly lower (25.6%) in patients wit…

OncologyMaleOrganoplatinum CompoundsOxaloacetatesPhysiologyColorectal cancerSettore MED/06 - Oncologia MedicavirusesClinical BiochemistryCellLeucovorinPromyelocytic Leukemia Proteinmedicine.disease_causeDeoxycytidineAntineoplastic Combined Chemotherapy Protocolsbiologyvirus diseasesNuclear ProteinsMiddle AgedOxaliplatinSurvival Ratemedicine.anatomical_structureImmunohistochemistryoxaliplatin/fluoropyrimidineFemaleFluorouracilColorectal Neoplasmsmedicine.drugAdultmedicine.medical_specialtyAntimetabolites AntineoplasticPML; oxaliplatin/fluoropyrimidine; colorectal cancerAntineoplastic Agentscolorectal cancerPromyelocytic leukemia proteinPredictive Value of TestsInternal medicinemedicineHumansCapecitabineAgedRetrospective StudiesPMLbusiness.industryTumor Suppressor ProteinsRetrospective cohort studyCell Biologymedicine.diseaseOxaliplatinApoptosisDrug Resistance Neoplasmbiology.proteinCarcinogenesisbusinessTranscription Factors
researchProduct

p63 Isoforms Regulate Metabolism of Cancer Stem Cells

2014

p63 is an important regulator of epithelial development expressed in different variants containing (TA) or lacking (ΔN) the N-terminal transactivation domain. The different isoforms regulate stem-cell renewal and differentiation as well as cell senescence. Several studies indicate that p63 isoforms also play a role in cancer development; however, very little is known about the role played by p63 in regulating the cancer stem phenotype. Here we investigate the cellular signals regulated by TAp63 and ΔNp63 in a model of epithelial cancer stem cells. To this end, we used colon cancer stem cells, overexpressing either TAp63 or ΔNp63 isoforms, to carry out a proteomic study by chemical-labeling …

Gene isoformProteomicsProteomeRegulatorBiologyProteomicsBiochemistryTransactivationCancer stem cellmedicineHumansMetabolomicsProtein IsoformsProtein Interaction MapsSettore BIO/10 - BIOCHIMICAp63 colon cancer stem cells proteomics stable isotope dimethyl labeling glucose metabolismSettore BIO/12Tumor Suppressor ProteinsCancerGeneral Chemistrymedicine.diseasePhenotypePeptide FragmentsCell biologyIsotope LabelingNeoplastic Stem CellsStem cellSignal TransductionTranscription Factors
researchProduct

Heat shock and Cd2+ exposure regulate PML and Daxx release from ND10 by independent mechanisms that modify the induction of heat-shock proteins 70 an…

2003

Nuclear domains called ND10 or PML bodies might function as nuclear depots by recruiting or releasing certain proteins. Although recruitment of proteins through interferon-induced upregulation and SUMO-1 modification level of PML had been defined, it is not known whether release of proteins is regulated and has physiological consequences. Exposure to sublethal environmental stress revealed a sequential release of ND10-associated proteins. Upon heat shock Daxx and Sp100 were released but PML remained, whereas exposure to subtoxic concentrations of CdCl2 induced the release of ND10-associated proteins, including PML, with Sp100 remaining in a few sites. In both cases,recovery times were simil…

Co-Repressor ProteinsMAP Kinase Signaling SystemMacromolecular SubstancesSUMO-1 ProteinPromyelocytic Leukemia ProteinMicePromyelocytic leukemia proteinDeath-associated protein 6Stress PhysiologicalHeat shock proteinEndopeptidasesAnimalsHSP70 Heat-Shock ProteinsEnzyme InhibitorsHeat shockTranscription factorCells CulturedHeat-Shock ProteinsbiologyTumor Suppressor ProteinsIntracellular Signaling Peptides and ProteinsNuclear ProteinsCell BiologyCell Nucleus StructuresNeoplasm ProteinsCell biologyHsp70Cysteine EndopeptidasesEukaryotic CellsGene Expression RegulationImmunologybiology.proteinSignal transductionCarrier ProteinsCo-Repressor ProteinsHeat-Shock ResponseCadmiumMolecular ChaperonesTranscription FactorsJournal of Cell Science
researchProduct

E4BP4/NFIL3 modulates the epigenetically repressed RAS effector RASSF8 function through histone methyltransferases

2018

RAS proteins are major human oncogenes, and most of the studies are focused on enzymatic RAS effectors. Recently, nonenzymatic RAS effectors (RASSF, RAS association domain family) have garnered special attention because of their tumor-suppressive properties in contrast to the oncogenic potential of the classical enzymatic RAS effectors. Whereas most members of RASSF family are deregulated by promoter hypermethylation, RASSF8 promoter remains unmethylated in many cancers but the mechanism(s) of its down-regulation remains unknown. Here, we unveil E4BP4 as a critical transcriptional modulator repressing RASSF8 expression through histone methyltransferases, G9a and SUV39H1. In line with these …

0301 basic medicineTumor suppressor geneBreast NeoplasmsBiologyBiochemistryEpigenesis Genetic03 medical and health sciences0302 clinical medicineHistocompatibility AntigensHistone methylationHumansEpigeneticsMolecular BiologySUV39H1EffectorTumor Suppressor ProteinsNFIL3Molecular Bases of DiseaseCell BiologyHistone-Lysine N-MethyltransferaseMethyltransferasesCell biologyNeoplasm ProteinsGene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologyBasic-Leucine Zipper Transcription FactorsHEK293 Cells030220 oncology & carcinogenesisHistone methyltransferaseMCF-7 CellsFemaleFunction (biology)
researchProduct