Search results for "DM2"

showing 10 items of 39 documents

Effects of the MDM2 inhibitor Nutlin-3a on sensitivity of pancreatic cancer cells to berberine and modified berberines in the presence and absence of…

2021

Abstract Approaches to improve pancreatic cancer therapy are essential as this disease has a very bleak outcome. Approximately 80% of pancreatic cancers are pancreatic ductal adenocarcinomas (PDAC). A key regulatory gene frequently mutated (∼75%) in PDAC is the TP53 tumor suppressor gene which controls the transcription of multiple genes involved in cell cycle progression, apoptosis, cancer progression and other growth regulatory processes. The mouse double minute 2 homolog (MDM2) gene product is a nuclear-localized E3 ubiquitin ligase and negatively regulates the TP53 protein which results in its proteasomal degradation. Various MDM2 inhibitors have been isolated and examined in clinical t…

Nutlin-3aCancer ResearchBerberineendocrine system diseasesTumor suppressor geneNAX compoundsApoptosisPiperazinesTargeted therapyGene productCell Line TumorPancreatic cancerGeneticsmedicineHumansTP53neoplasmsMolecular BiologyRegulator geneNAX compundsbiologyChemistryImidazolesPDACCancerProto-Oncogene Proteins c-mdm2PDCAmedicine.diseaseUbiquitin ligasePancreatic NeoplasmsCell culturebiology.proteinCancer researchNAX compoundMolecular MedicineMdm2Tumor Suppressor Protein p53Signal TransductionAdvances in Biological Regulation
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CASP8 SNP D302H (rs1045485) is associated with worse survival in MYCN-amplified neuroblastoma patients

2014

Background Neuroblastoma is a pediatric cancer that exhibits a wide clinical spectrum ranging from spontaneous regression in low-risk patients to fatal disease in high-risk patients. The identification of single nucleotide polymorphisms (SNPs) may help explain the heterogeneity of neuroblastoma and assist in identifying patients at higher risk for poor survival. SNPs in the TP53 pathway are of special importance, as several studies have reported associations between TP53 pathway SNPs and cancer. Of note, less than 2% of neuroblastoma tumors have a TP53 mutation at diagnosis. Patients and Methods We selected 21 of the most frequently studied SNPs in the TP53 pathway and evaluated their assoc…

OncologyGenotyping TechniquesMedizinlcsh:MedicineGenome-wide association studyPROGRESSIONSUSCEPTIBILITYBioinformaticsNeuroblastomaCHEMOSENSITIVITYMedicine and Health SciencesMissense mutationlcsh:ScienceOncogene ProteinsCaspase 8N-Myc Proto-Oncogene ProteinMultidisciplinaryCELL-LINENuclear ProteinsCANCERAPOPTOSISGENOTYPEGene Expression Regulation NeoplasticResearch Articlemedicine.medical_specialtySingle-nucleotide polymorphismBiologyN-Myc Proto-Oncogene ProteinPolymorphism Single NucleotideDisease-Free SurvivalMDM2 SNP309Molecular GeneticsNeuroblastomaInternal medicineCASPASE-8medicineGeneticsCancer GeneticsSNPHumansneoplasmsNeoplasm StagingClinical GeneticsP53lcsh:RGene AmplificationCancerInfantBiology and Life Sciencesmedicine.diseasePediatric cancerGeriatricsGenetics of Diseaselcsh:Q
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Molecular and immunohistochemical analysis of the prognostic value of cell-cycle regulators in urothelial neoplasms of the bladder.

2006

Abstract Objective To evaluate the prognostic and predictive value of molecular and immunohistochemical markers related to cell-cycle control in terms of recurrence, progression, and survival in urothelial neoplasms of the bladder (UNB). Patients and Methods Clinical and pathological findings of 84 patients with UNB were assessed. Homozygous deletion (HD) and promoter methylation of p14 ARF , p15 INK4B , p16 INK4A , loss of heterozygosity of the locus 9p21, p53 mutations, and immunohistochemical expression of p53, p16, p14, p21, p27, pRb, Ki67, MDM2, and cyclin D1 proteins were evaluated in relation to overall survival (OS), recurrence-free survival (RFS), and progression-free survival (PFS…

OncologyMalemedicine.medical_specialtyUrologyCell Cycle ProteinsLoss of heterozygosityCyclin D1p14arfPredictive Value of TestsInternal medicineTumor Suppressor Protein p14ARFmedicineBiomarkers TumorHumansCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15Univariate analysisBladder cancerbusiness.industryCarcinomaRetinoblastomaAnatomical pathologyProto-Oncogene Proteins c-mdm2Cell cyclemedicine.diseasePrognosisImmunohistochemistrySurvival AnalysisKi-67 AntigenMolecular Diagnostic TechniquesUrinary Bladder NeoplasmsCancer researchDisease ProgressionImmunohistochemistryFemaleNeoplasm Recurrence LocalTumor Suppressor Protein p53UrotheliumbusinessCyclin-Dependent Kinase Inhibitor p27European urology
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Primary glioblastomas with and without EGFR amplification: Relationship to genetic alterations and clinicopathological features

2009

Glioblastomas express a notable heterogeneity in both the histological and cell patterns with glial astrocytic differentiation. Primary glioblastoma, which is the most frequent presentation (90-95%), occurs mainly in older patients and arises de novo, without any clinical or histological evidence of a less malignant precursor lesion. EGFR amplification has been identified as a genetic hallmark of primary glioblastomas and occurs in 40-60% of cases. However, there exist primary glioblastomas without EGFR amplification/overexpression. The purpose of this study was to stabilize the association between cases with and without EGFR gene amplification with clinical and genetic parameters in 45 cas…

Pathologymedicine.medical_specialtyEGFR AmplificationCellGeneral MedicineBiologyTp53 mutationmedicine.diseasePathology and Forensic Medicinemedicine.anatomical_structureOlder patientsCancer researchmedicinebiology.proteinClinicopathological featuresMdm2EGFR Gene AmplificationNeurology (clinical)neoplasmsGlioblastomaNeuropathology
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Molecular Alterations of the RBI, TP53, and MDM2 Genes in Primary and Xenografted Human Osteosarcomas

1997

We report the status of the RBI, TP53, and MDM2 genes in human osteosarcomas and cell lines established from surgical specimens and transplanted into athymic naked mice. By using reverse transcriptase-polymerase chain reaction (RT-PCR) as a prescreening technique and posterior sequencing, we observe

Primary (chemistry)Cell cultureCancer researchbiology.proteinMdm2Cell BiologyBiologyneoplasmsMolecular BiologyGenePathology and Forensic MedicineDiagnostic Molecular Pathology
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Molecular dynamics studies on Mdm2 complexes: An analysis of the inhibitor influence

2012

p53 is a powerful anti-tumoral molecule frequently inactivated by mutations or deletions in cancer. However, half of all human tumors expresses wild-type p53, and its activation, by antagonizing its negative regulator Mdm2, might offer a new strategy for therapeutic protocol. In this work, we present a molecular dynamics study on Mdm2 structure bound to two different known inhibitors with the aim to investigate the structural transitions between apo-Mdm2 and Mdm2-inhibitor complexes. We tried to gain information about conformational changes binding a benzodiazepine derivative inhibitor with respect the known nutlin and the apo form. The conformational changes alter the size of the cleft and…

Protein ConformationBiophysicsMolecular Dynamics SimulationMdm2 p53 nutlin benzodiazepine Molecular DynamicsBiochemistryNegative regulatorBenzodiazepineschemistry.chemical_compoundMolecular dynamicsHumansMoleculeEnzyme InhibitorsMolecular BiologyBinding SitesbiologyChemistryProto-Oncogene Proteins c-mdm2Cell BiologyNutlinSettore CHIM/08 - Chimica FarmaceuticaBiochemistryDrug DesignBiophysicsbiology.proteinMdm2LinkerBiochemical and Biophysical Research Communications
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Parthenolide sensitizes hepatocellular carcinoma cells to trail by inducing the expression of death receptors through inhibition of STAT3 activation

2011

This article shows that HepG2, Hep3B, and SK-Hep1 cells, three lines of human hepatocellular carcinoma (HCC) cells, are resistant to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Parthenolide, a sesquiterpene lactone found in European feverfew, has been shown to exert both anti-inflammatory and anti-cancer activities. This article demonstrates that co-treatment with parthenolide and TRAIL-induced apoptosis with synergistic interactions in the three lines of HCC cells. In order to explain these effects we ascertained that parthenolide increased either at protein or mRNA level the total content of death receptors TRAIL-R1 and -R2 as well as their surfac…

STAT3 Transcription FactorCarcinoma HepatocellularPhysiologyClinical BiochemistryCellDown-RegulationTRAILApoptosisPharmacologyParthenolideSTAT3TNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSettore BIO/10 - BiochimicamedicineHumansParthenolidePhosphorylationReceptorSTAT3CaspaseJanus KinasesbiologyLiver NeoplasmsProto-Oncogene Proteins c-mdm2Hep G2 CellsReceptors Death DomainCell BiologyapoptosiEnzyme ActivationGene Expression Regulation Neoplasticmedicine.anatomical_structurechemistryCell cultureApoptosisCaspasesbiology.proteinSTAT proteinDrug Screening Assays AntitumorTumor Suppressor Protein p53SesquiterpenesJournal of Cellular Physiology
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A Regulatory Mechanism Involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the Control of Cell Proliferation

2011

Abstract TBP-1 /Tat-Binding Protein 1 (also named Rpt-5, S6a or PSMC3) is a multifunctional protein, originally identified as a regulator of HIV-1-Tat mediated transcription. It is an AAA-ATPase component of the 19S regulative subunit of the proteasome and, as other members of this protein family, fulfils different cellular functions including proteolysis and transcriptional regulation. We and others reported that over expression of TBP-1 diminishes cell proliferation in different cellular contexts with mechanisms yet to be defined. Accordingly, we demonstrated that TBP-1 binds to and stabilizes the p14ARF oncosuppressor increasing its anti-oncogenic functions. However, TBP-1 restrains cell…

TBP-1/Tat-Binding Protein 1lcsh:Medicinemacromolecular substancesBiologymTORC2Cell GrowthTBP-1/Tat-Binding Protein 1; cell proliferationp14arfMolecular Cell BiologyGeneticsCancer GeneticsTranscriptional regulationGene Networkslcsh:ScienceBiologyProtein kinase BPI3K/AKT/mTOR pathwayMultidisciplinaryCell growthAKTBinding proteinlcsh:RMolecular biologySignaling CascadesCell biologyTBP-1enzymes and coenzymes (carbohydrates)cell proliferationbiology.proteinMdm2lcsh:QCell DivisionResearch ArticleSignal TransductionPLoS ONE
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Paclitaxel and beta-lapachone synergistically induce apoptosis in human retinoblastoma Y79 cells by downregulating the levels of phospho-Akt.

2009

Paclitaxel (PTX) and beta-lapachone (LPC) are naturally occurring compounds that have shown a large spectrum of anticancer activity. In this article we show for the first time that PTX/LPC combination induces potent synergistic apoptotic effects in human retinoblastoma Y79 cells. Combination of suboptimal doses of PTX (0.3 nM) and LPC (1.5 microM) caused biochemical and morphological signs of apoptosis at 48 h of treatment. These effects were accompanied by potent lowering in inhibitor of apoptosis proteins and by activation of Bid and caspases 3 and 6 with lamin B and PARP breakdown. PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM…

Time FactorsPhysiologyClinical BiochemistryApoptosisInhibitor of Apoptosis ProteinsWortmanninchemistry.chemical_compoundSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsPhosphorylationCaspasebiologyCaspase 6Lamin Type BCaspase 3Protein StabilityRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2TransfectionBiochemistrylipids (amino acids peptides and proteins)Poly(ADP-ribose) PolymerasesWortmanninBH3 Interacting Domain Death Agonist Proteinretinoblastoma survival factors apoptosisPaclitaxelCell SurvivalPoly ADP ribose polymeraseActive Transport Cell NucleusDown-RegulationInhibitor of apoptosisTransfectionCell Line TumorHumansProtein kinase BProtein Kinase InhibitorsCell NucleusDose-Response Relationship DrugCell BiologyAntineoplastic Agents PhytogenicAndrostadieneschemistryCell cultureApoptosisbiology.proteinCancer researchTumor Suppressor Protein p53Proto-Oncogene Proteins c-aktNaphthoquinonesJournal of cellular physiology
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Insulin-like growth factor 1 differentially regulates estrogen receptor-dependent transcription at estrogen response element and AP-1 sites in breast…

2007

Cross-talk between insulin-like growth factor 1 (IGF-1) and estrogen receptor alpha (ER) regulates gene expression in breast cancer cells, but the underlying mechanisms remain unclear. Here, we studied how 17-beta-estradiol (E2) and IGF-1 affect ER transcriptional machinery in MCF-7 cells. E2 treatment stimulated ER loading on the estrogen response element (ERE) in the pS2 promoter and on the AP-1 motif in the cyclin D1 promoter. On ERE, similar amounts of liganded ER were found at 1-24-h time points, whereas on AP-1, ER binding fluctuated over time. At 1 h, liganded ER was recruited to ERE together with histone acetyltransferases SRC-1 and p300, ubiquitin ligase E6-AP, histone methyltransf…

Transcription GeneticActive Transport Cell NucleusEstrogen receptorBreast NeoplasmsLigandsResponse ElementsBiochemistryCyclin D1Cell Line TumorHumansCyclin D1RNA MessengerInsulin-Like Growth Factor IHistone H3 acetylationMolecular BiologyHormone response elementbiologyEstradiolTumor Suppressor ProteinsEstrogen Receptor alphaCell BiologyUbiquitin ligaseCell biologyUp-RegulationTranscription Factor AP-1Histone methyltransferasebiology.proteinCancer researchMdm2Trefoil Factor-1Estrogen receptor alphahormones hormone substitutes and hormone antagonistsThe Journal of biological chemistry
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