Search results for "protein p53"

showing 10 items of 201 documents

Low doses of paclitaxel potently induce apoptosis in human retinoblastoma Y79 cells by up-regulating E2F1.

2008

Paclitaxel (PTX) is an anticancer drug currently in phase II clinical trials. This study shows for the first time that low doses of PTX (5 nM) potently induce apoptosis in human retinoblastoma Y79 cells. The effect of PTX is accompanied by a potent induction of E2F1 which appears to play a critical role in the effects induced by PTX. PTX induced a dose- and time-dependent effect, with G2/M arrest, cyclines A, E and B1 accumulation and a marked modification in the status of Cdc2-cyclin B1 complex, the major player of the G2/M checkpoint. Apoptosis followed G2/M arrest. An early and prolonged increase in p53 expression with its stabilization by phosphorylation and acetylation and its nuclear …

Cyclin-Dependent Kinase Inhibitor p21G2 Phaseendocrine systemCancer ResearchProgrammed cell deathPaclitaxelApoptosisBiologyretinoblastoma apoptosis paclitaxelp14arfSettore BIO/10 - BiochimicaCell Line TumorE2F1HumansFragmentation (cell biology)PhosphorylationMembrane Potential MitochondrialRetinoblastomaCell cycleAntineoplastic Agents PhytogenicUp-RegulationGene Expression Regulation NeoplasticOncologyApoptosisCancer researchPhosphorylationApoptosomeTumor Suppressor Protein p53Cell DivisionE2F1 Transcription FactorInternational journal of oncology
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Loss of Neuroglobin Expression Alters Cdkn1a/Cdk6-Expression Resulting in Increased Proliferation of Neural Stem Cells

2018

Abstract: In the quest to unravel its functional significance, neuroglobin (Ngb), a brain-specific neuroprotective protein, has recently been proposed as an actor in neurodevelopment. As neural stem cells (NSCs) are fundamental during brain development, the present study aimed at investigating the role of Ngb in the growth and proliferation of NSCs by comparing an Ngb-floxed (Ngb(fl)-)NSC line, equivalent to the wild-type cellular situation, with an in-house created Ngb knockout (Ngb(KO)-)NSC line. Ngb(KO)-NSCs were characterized by an increased growth and proliferation capacity in vitro, supported by RNA sequencing and western blot results reporting the downregulation of Cdkn1a and the upr…

Cyclin-Dependent Kinase Inhibitor p21Male0301 basic medicineCell signalingDown-RegulationNeuroglobinNerve Tissue ProteinsBiologyNeuroprotectionTranscriptomeMice03 medical and health sciences0302 clinical medicineNeural Stem CellsDownregulation and upregulationAnimalsBiologyCells CulturedCell ProliferationCell CycleCyclin-Dependent Kinase 6Cell BiologyHematologyCell cycleNeural stem cellUp-RegulationCell biologyMice Inbred C57BL030104 developmental biologynervous systemNeuroglobinbiology.proteinFemaleHuman medicineCyclin-dependent kinase 6Tumor Suppressor Protein p53Proto-Oncogene Proteins c-akt030217 neurology & neurosurgerySignal TransductionDevelopmental BiologyStem Cells and Development
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Prognostic Significance of Histopathological Grading and Immunoreactivity for p53 and p21/WAF1 in Grade 2 pTa Transitional Cell Carcinoma of …

2001

At present, there are no predictors of tumour behaviour for grade (G) 2 pTa transitional cell carcinomas (TCC) of the bladder. Here we analyse the prognostic relevance of histopathological grading and the immunohistochemical detection of p53 and p21/WAF1.70 patients were newly diagnosed with G2 pTa TCC of the bladder based on transurethral resection specimens. Two pathologists, blinded with respect to the clinical outcome, confirmed the initial grade and subclassified the G2 lesions into G2a and G2b carcinomas based on the degree of nuclear atypia and the number of mitoses. Immunoreactivity for p53 and p21/WAF1 was evaluated semiquantitatively.There were 52 G2a and 18 G2b tumours, mean foll…

Cyclin-Dependent Kinase Inhibitor p21Pathologymedicine.medical_specialtyUrologyHistopathological gradingurologic and male genital diseasesCyclinsotorhinolaryngologic diseasesHumansMedicineGrading (tumors)Neoplasm StagingCarcinoma Transitional CellUrinary bladderbusiness.industryPrognosismedicine.diseasefemale genital diseases and pregnancy complicationsP21 waf1medicine.anatomical_structureTransitional cell carcinomaUrinary Bladder NeoplasmsTransitional CellImmunohistochemistryNeoplasm stagingTumor Suppressor Protein p53businessEuropean Urology
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Activated kRas protects colon cancer cells from cucurbitacin-induced apoptosis: The role of p53 and p21

2008

Cucurbitacins have been shown to inhibit proliferation in a variety of cancer cell lines. The aim of this study was to determine their biological activity in colon cancer cell lines that do not harbor activated STAT3, the key target of cucurbitacin. In order to establish the role of activated kRas in the responsiveness of cells to cucurbitacins, we performed experiments in isogenic colon cancer cell lines, HCT116 and Hke-3, which differ only by the presence of an activated kRas allele. We compared the activity of 23, 24-dihydrocucurbitacin B (DHCB) and cucurbitacin R (CCR), two cucurbitacins that we recently isolated, with cucurbitacin I (CCI), a cucurbitacin with established antitumorigeni…

Cyclin-Dependent Kinase Inhibitor p21Programmed cell deathTumor suppressor geneAntineoplastic AgentsApoptosisBiologymedicine.disease_causeBiochemistryArticleProto-Oncogene Proteins p21(ras)CucurbitacinsCell Line TumorProto-Oncogene ProteinsmedicineHumansCell ProliferationPharmacologyCell growthCucurbitacinTriterpenesdigestive system diseasesCell cultureApoptosisColonic Neoplasmsras ProteinsCancer researchKRASTumor Suppressor Protein p53Biochemical Pharmacology
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The role of reactive oxygen species and subsequent DNA-damage response in the emergence of resistance towards resveratrol in colon cancer models

2014

AbstractIn spite of the novel strategies to treat colon cancer, mortality rates associated with this disease remain consistently high. Tumour recurrence has been linked to the induction of resistance towards chemotherapy that involves cellular events that enable cancer cells to escape cell death. Treatment of colon cancer mainly implicates direct or indirect DNA-damaging agents and increased repair or tolerances towards subsequent lesions contribute to generate resistant populations. Resveratrol (RSV), a potent chemosensitising polyphenol, might share common properties with chemotherapeutic drugs through its indirect DNA-damaging effects reported in vitro. In this study, we investigated how…

Cyclin-Dependent Kinase Inhibitor p21SenescenceCancer ResearchProgrammed cell deathColonDNA damageColorectal cancerImmunologyApoptosisBiologyResveratrolS PhaseHistonesPolyploidyCellular and Molecular Neurosciencechemistry.chemical_compoundCell Line TumorStilbenesmedicineAnimalsHumansCHEK1Cyclin-Dependent Kinase Inhibitor p16Cell Biologymedicine.diseaseAntineoplastic Agents PhytogenicRatsGene Expression Regulation NeoplasticCheckpoint Kinase 2chemistryDrug Resistance NeoplasmResveratrolApoptosisCheckpoint Kinase 1Cancer cellImmunologyCancer researchOriginal ArticleTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein KinasesDNA DamageSignal TransductionCell Death & Disease
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In vivo studies of altered expression patterns of p53 and proliferative control genes in chronic vitamin A deficiency and hypervitaminosis

2003

Several clinical trials have revealed that individuals who were given beta-carotene and vitamin A did not have a reduced risk of cancer compared to those given placebo; rather, vitamin A could actually have caused an adverse effect in the lungs of smokers [Omenn, G.S., Goodman, G.E., Thornquist, M.D., Balmes, J., Cullen, M.R., Glass, A., Keogh, J.P., Meyskens, F.L., Valanis, B., Williams, J.H., Barnhart, S. & Hammar, S. N. Engl. J. Med (1996) 334, 1150-1155; Hennekens, C.H., Buring, J.E., Manson, J.E., Stampfer, M., Rosner, B., Cook, N.R., Belanger, C., LaMotte, F., Gaziano, J.M., Ridker, P.M., Willet, W. & Peto, R. (1996) N. Engl. J. Med. 334, 1145-1149]. Using differential display techniq…

Cyclin-Dependent Kinase Inhibitor p21VitaminRetinyl Estersmedicine.medical_specialtyMacromolecular SubstancesProto-Oncogene Proteins c-junReceptors Retinoic AcidBlotting WesternRetinoic acidBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundIn vivoCyclinsInternal medicinemedicineAnimalsHypervitaminosis ARNA MessengerRats WistarVitamin AReceptorLungDifferential displayReverse Transcriptase Polymerase Chain ReactionVitamin A DeficiencyGene Expression ProfilingDNAmedicine.diseaseHypervitaminosisPrecipitin TestsRatsVitamin A deficiencyEndocrinologyGene Expression RegulationLiverchemistryChronic DiseaseImmunologyDiterpenesTumor Suppressor Protein p53CarcinogenesisCell DivisionEuropean Journal of Biochemistry
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Prognostic Value of p53, p21/WAF1, Bcl-2, Bax, Bak and Ki-67 Immunoreactivity in pT1 G3 Urothelial Bladder Carcinomas

2001

pT1 G3 bladder carcinomas are heterogeneous with respect to tumor recurrence and progression. Whereas some urologists treat these carcinomas by repeated transurethral resections often followed by intravesical chemotherapy or BCG instillation, others recommend cystectomy after tumor recurrence or early cystectomy after the initial diagnosis. Our goal was to determine the prognostic value of p53, p21/WAF1, Bcl-2, Bax, Bak, and Ki-67 immunoreactivity in these tumors. There were 30 patients with a new histopathological diagnosis of pT1 G3 urothelial carcinoma based on a transurethral resection specimen. Representative sections of these specimens were examined for the above markers. All patients…

Cyclin-Dependent Kinase Inhibitor p21medicine.medical_specialtyPathologyTime FactorsTumor suppressor genemedicine.medical_treatmentBcl 2 baxUrologyDisease-Free SurvivalCystectomyPredictive Value of TestsCyclinsProto-Oncogene ProteinsBiomarkers TumormedicineHumansNeoplasm InvasivenessRetrospective Studiesbcl-2-Associated X ProteinCarcinoma Transitional CellUrinary bladderBladder cancerbiologyMembrane ProteinsGeneral MedicinePrognosismedicine.diseaseImmunohistochemistrySurvival RateKi-67 Antigenbcl-2 Homologous Antagonist-Killer Proteinmedicine.anatomical_structureTransitional cell carcinomaProto-Oncogene Proteins c-bcl-2Urinary Bladder NeoplasmsTumor progressionKi-67biology.proteinTumor Suppressor Protein p53Follow-Up StudiesTumor Biology
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Upregulation of Major Histocompatibility Complex Class I on Liver Cells by Hepatitis C Virus Core Protein via p53 and TAP1 Impairs Natural Killer Cel…

2003

ABSTRACTThe mechanisms of immune evasion and the role of the early immune response in chronic infection caused by hepatitis C virus (HCV) are still unclear. Here, we present evidence for a cascade of molecular events that the virus initiates to subvert the innate immune attack. The HCV core protein induced p53-dependent gene expression of TAP1 (transporter associated with antigen processing 1) and consecutive major histocompatibility complex (MHC) class I upregulation. Moreover, in p53-deficient liver cell lines, only reconstitution with wild-type p53, but not mutated p53 lacking DNA binding capacity, showed this effect. As a consequence of increased MHC class I expression, a significantly …

Cytotoxicity ImmunologicImmunologyAntigen presentationHepacivirusMajor histocompatibility complexMicrobiologyCell LineNatural killer cellAntigenVirologyMHC class ImedicineHumansATP Binding Cassette Transporter Subfamily B Member 2Cells CulturedLymphokine-activated killer cellbiologyViral Core ProteinsHistocompatibility Antigens Class IHepatitis C ChronicNatural killer T cellVirologyUp-RegulationKiller Cells Naturalmedicine.anatomical_structureInsect ScienceImmunologyHepatocytesbiology.proteinPathogenesis and ImmunityATP-Binding Cassette TransportersTumor Suppressor Protein p53CD8Journal of Virology
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The sequence alteration associated with a mutational hotspot in p53 protects cells from lysis by cytotoxic T lymphocytes specific for a flanking pept…

1998

A high proportion of tumors arise due to mutation of the p53 tumor suppressor protein. A p53 hotspot mutation at amino acid position 273 from R to H, flanking a peptide epitope that spans residues 264–272, renders cells resistant to killing by human histocompatibility leukocyte antigen (HLA)-A*0201–restricted cytotoxic T lymphocytes (CTLs) specific for this epitope. Acquisition of the R to H mutation at residue 273 of the human p53 protein promotes tumor growth in vivo by selective escape from recognition by p53.264–272 peptide-specific CTLs. Synthetic 27-mer p53 polypeptides covering the antigenic nonamer region 264–272 of p53 were used as proteasome substrates to investigate whether the R…

Cytotoxicity Immunologicp53Epitopes T-LymphocyteEpitopeSubstrate SpecificityMice0302 clinical medicineTumor Cells CulturedImmunology and AllergyCytotoxic T cellPeptide sequence0303 health sciencesAntigen PresentationproteasomesHydrolysisArticles3. Good healthCysteine Endopeptidasestumor antigensCell DivisionProteasome Endopeptidase ComplexImmunologyAntigen presentationMolecular Sequence DataMice TransgenicBiologyArgininecytotoxic T lymphocytes03 medical and health sciencesAntigenMultienzyme Complexesantigen processingAnimalsHumansPoint MutationHistidineAmino Acid Sequence030304 developmental biologyBinding SitesLinear epitopeHLA-A AntigensPoint mutationCytotoxicity Tests ImmunologicMolecular biologyPeptide FragmentsCTL*Tumor Suppressor Protein p53Peptides030215 immunologyT-Lymphocytes CytotoxicThe Journal of experimental medicine
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Cell proliferation and DNA breaks are involved in ultraviolet light-induced apoptosis in nucleotide excision repair-deficient Chinese hamster cells.

2002

UV light targets both membrane receptors and nuclear DNA, thus evoking signals triggering apoptosis. Although receptor-mediated apoptosis has been extensively investigated, the role of DNA damage in apoptosis is less clear. To analyze the importance of DNA damage induced by UV-C light in apoptosis, we compared nucleotide excision repair (NER)-deficient Chinese hamster ovary cells (lines 27-1 and 43-3B mutated for the repair genes ERCC3 and ERCC1, respectively) with the corresponding DNA repair-proficient fibroblasts (CHO-9 and ERCC1 complemented 43-3B cells). NER-deficient cells were hypersensitive as to the induction of apoptosis, indicating that apoptosis induced by UV-C light is due to u…

DNA RepairTranscription GeneticDNA repairDNA damageCell SurvivalUltraviolet RaysApoptosisCHO CellsBiologyCysteine Proteinase InhibitorsRadiation ToleranceArticleMiceCricetinaeUltraviolet lightAnimalsMolecular BiologyChromosome AberrationsIntrinsic apoptosisCell CycleDNA replicationCell BiologyFibroblastsMolecular biologyCaspase InhibitorsChromatinCell biologyKineticsUVB-induced apoptosisProto-Oncogene Proteins c-bcl-2ApoptosisMutationTumor Suppressor Protein p53Cell DivisionNucleotide excision repairDNA DamageMolecular biology of the cell
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