Search results for "Tumor suppressor gene"

showing 10 items of 98 documents

Cytotoxicity of sesquiterpene alkaloids from Nuphar plants toward sensitive and drug-resistant cell lines.

2018

Multi-drug resistance (MDR) is a critical problem in cancer chemotherapy. MDR causes the overexpression of ATP-binding cassette (ABC) transporters and mutations in tumor suppressor genes and oncogenes. To tackle this issue, in this study, we focused on Nuphar plants, which have been traditionally used as food. Sesquiterpene alkaloids (1–3) were isolated from N. japonicum and dimeric sesquiterpene thioalkaloids (4–10) were isolated from N. pumilum. P-glycoprotein-overexpressing CEM/ADR5000 cells were cross-resistant to 6,6′-dihydroxythiobinupharidine (10). Using in silico molecular docking, we calculated the binding energies and simulated the interactions of these compounds with the correspo…

0301 basic medicineATP Binding Cassette Transporter Subfamily BTumor suppressor geneCell SurvivalATP-binding cassette transporterNuphar03 medical and health sciences0302 clinical medicineAlkaloidsCell Line TumorNeoplasmsATP Binding Cassette Transporter Subfamily G Member 2HumansATP Binding Cassette Transporter Subfamily B Member 1Binding siteCytotoxicityGeneOncogeneChemistryPlant ExtractsABCB5General MedicineMolecular biologyAntineoplastic Agents PhytogenicNeoplasm ProteinsGene Expression Regulation NeoplasticMolecular Docking Simulation030104 developmental biologyCell cultureDrug Resistance Neoplasm030220 oncology & carcinogenesisSesquiterpenesFood ScienceFoodfunction
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Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling

2017

The pathogenesis of chronic lymphocytic leukemia (CLL) has been linked to constitutive NF-κB activation but the underlying mechanisms are poorly understood. Here we show that alternative splicing of the negative regulator of NF-κB and tumor suppressor gene CYLD regulates the pool of CD5+ B cells through sustained canonical NF-κB signaling. Reinforced canonical NF-κB activity leads to the development of B1 cell-associated tumor formation in aging mice by promoting survival and proliferation of CD5+ B cells, highly reminiscent of human B-CLL. We show that a substantial number of CLL patient samples express sCYLD, strongly implicating a role for it in human B-CLL. We propose that our new CLL-l…

0301 basic medicineCancer ResearchTumor suppressor geneCell SurvivalRNA SplicingChronic lymphocytic leukemia2720 Hematology610 Medicine & healthBiologyCD5 Antigenslaw.inventionPathogenesisMice03 medical and health sciencesimmune system diseaseslawhemic and lymphatic diseasesmedicineAnimalsHumans10239 Institute of Laboratory Animal Science1306 Cancer ResearchGenes Tumor SuppressorGeneCell ProliferationB-LymphocytesAlternative splicingNF-kappa BUbiquitinationHematologymedicine.diseaseLeukemia Lymphocytic Chronic B-CellDeubiquitinating Enzyme CYLDLeukemia030104 developmental biologyOncologyImmunologyCancer research570 Life sciences; biologySuppressor2730 OncologyCD5Signal TransductionLeukemia
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Roles of TP53 in determining therapeutic sensitivity, growth, cellular senescence, invasion and metastasis.

2016

TP53 is a critical tumor suppressor gene that regulates cell cycle progression, apoptosis, cellular senescence and many other properties critical for control of normal cellular growth and death. Due to the pleiotropic effects that TP53 has on gene expression and cellular physiology, mutations at this tumor suppressor gene result in diverse physiological effects. T53 mutations are frequently detected in numerous cancers. The expression of TP53 can be induced by various agents used to treat cancer patients such as chemotherapeutic drugs and ionizing radiation. Radiation will induce Ataxia telangiectasia mutated (ATM) and other kinases that results in the phosphorylation and activation of TP53…

0301 basic medicineCancer Researchendocrine system diseasesMetastasimedicine.disease_causeMetastasisAntineoplastic AgentInvasionNeoplasmsTP53Neoplasm Metastasisbcl-2-Associated X ProteinAza CompoundProto-Oncogene ProteinApoptosis Regulatory ProteinbiologyCell CyclemiRMicroRNACell cycleCell biologyNeoplasm MetastasiGene Expression Regulation NeoplasticNutlin-3 chemosensitivityMdm2Molecular MedicineHumanSignal TransductionCyclin-Dependent Kinase Inhibitor p21Tumor suppressor genemiRsAntineoplastic AgentsCellular senescenceTP53; miRs; MDM2; Nutlin-3 chemosensitivity; Cellular senescence ; Invasion; Metastasis03 medical and health sciencesBcl-2-associated X proteinGeneticMDM2Proto-Oncogene ProteinsmicroRNAGeneticsmedicineHumansNeoplasm InvasivenessneoplasmsMolecular BiologyCell ProliferationNeoplasm InvasiveneAza CompoundsOncomirBridged Bicyclo Compounds HeterocyclicMicroRNAs030104 developmental biologyTumor progressionbiology.proteinNeoplasmTumor Suppressor Protein p53CarcinogenesisApoptosis Regulatory Proteins
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A PTEN inhibitor displays preclinical activity against hepatocarcinoma cells

2016

Phosphatase and tensin homolog (PTEN) gene is considered a tumor suppressor gene. However, PTEN mutations rarely occur in hepatocellular carcinoma (HCC), whereas heterozygosity of PTEN, resulting in reduced PTEN expression, has been observed in 32–44% of HCC patients. In the present study, we investigated the effects of the small molecule PTEN inhibitor VO-OHpic in HCC cells. VO-OHpic inhibited cell viability, cell proliferation and colony formation, and induced senescence-associated β-galactosidase activity in Hep3B (low PTEN expression) and to a lesser extent in PLC/PRF/5 (high PTEN expression) cells, but not in PTEN-negative SNU475 cells. VO-OHpic synergistically inhibited cell viability…

0301 basic medicineMAPK/ERK pathwayPTENCarcinoma HepatocellularsenescenceTumor suppressor geneCell SurvivalMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineReportOrganometallic CompoundsAnimalsHumansPTENTensinViability assayHCCProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationbiologyCell growthTOR Serine-Threonine KinasesAKTLiver NeoplasmsPTEN PhosphohydrolaseCell BiologySorafenibXenograft Model Antitumor Assaysdigestive system diseasesVO-OHpicGene Expression Regulation Neoplastic030104 developmental biology030220 oncology & carcinogenesisbiology.proteinCancer researchSignal TransductionDevelopmental Biology
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Pivotal roles of glycogen synthase-3 in hepatocellular carcinoma

2017

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world, and represents the second most frequently cancer and third most common cause of death from cancer worldwide. At advanced stage, HCC is a highly aggressive tumor with a poor prognosis and with very limited response to common therapies. Therefore, there is still the need for new effective and well-tolerated therapeutic strategies. Molecular-targeted therapies hold promise for HCC treatment. One promising molecular target is the multifunctional serine/threonine kinase glycogen synthase kinase 3 (GSK-3). The roles of GSK-3β in HCC remain controversial, several studies suggested a possible role of GSK-3β as a tumor …

0301 basic medicinePathologymedicine.medical_specialtyCancer ResearchCarcinoma HepatocellularEpithelial-Mesenchymal TransitionTumor suppressor geneAntineoplastic Agentsmacromolecular substancesBiologyMetastasisGlycogen Synthase Kinase 303 medical and health sciencesWnt0302 clinical medicineGeneticTransforming Growth Factor betaGSK-3GeneticsmedicineHumansHedgehog ProteinsMolecular Targeted TherapyInsulin-Like Growth Factor IHCCIGFβ-cateninGlycogen synthaseHedgehogMolecular Biologybeta CateninGSK-3Glycogen Synthase Kinase 3 betaReceptors NotchLiver NeoplasmsWnt signaling pathwayCancermedicine.diseaseSurvival Analysisdigestive system diseasesGene Expression Regulation Neoplastic030104 developmental biology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinCancer researchMolecular MedicineHedgehogSignal Transduction
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Pharmacogenomics of Scopoletin in Tumor Cells

2016

Drug resistance and the severe side effects of chemotherapy necessitate the development of novel anticancer drugs. Natural products are a valuable source for drug development. Scopoletin is a coumarin compound, which can be found in several Artemisia species and other plant genera. Microarray-based RNA expression profiling of the NCI cell line panel showed that cellular response of scopoletin did not correlate to the expression of ATP-binding cassette (ABC) transporters as classical drug resistance mechanisms (ABCB1, ABCB5, ABCC1, ABCG2). This was also true for the expression of the oncogene EGFR and the mutational status of the tumor suppressor gene, TP53. However, mutations in the RAS onc…

0301 basic medicinePharmaceutical ScienceATP-binding cassette transporterDrug resistancePharmacologycoumarinAnalytical Chemistrychemistry.chemical_compound0302 clinical medicineNeoplasmsDrug DiscoveryABC-transportermicroarraysNF-kappa BABCB5Drug Resistance MultipleGene Expression Regulation NeoplasticMolecular Docking SimulationDrug developmentChemistry (miscellaneous)030220 oncology & carcinogenesisherbal medicineMolecular MedicineSignal TransductionTumor suppressor geneProtein Array AnalysisBiologyArticlelcsh:QD241-44103 medical and health scienceslcsh:Organic chemistrymultidrug resistanceCell Line TumorScopoletinHumansPhysical and Theoretical ChemistryTranscription factorScopoletinOncogenePlant ExtractsOrganic ChemistryTranscription Factor RelAphytotherapy030104 developmental biologyArtemisiachemistryDrug Resistance NeoplasmPharmacogeneticsCancer researchABC-transporter; cluster analysis; coumarin; herbal medicine; microarrays; multidrug resistance; phytotherapyATP-Binding Cassette Transporterscluster analysisMolecules
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11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma

2020

High-risk 11q deleted neuroblastomas typically display undifferentiated/poorly differentiated morphology. Neuroblastoma is thought to develop from Schwann cell precursors and undifferentiated neural crest (NC) derived cells. It is therefore vital to understand mechanisms involved in the block of differentiation. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in maintenance of undifferentiated NC-derived progenitors via repression of DLG2, a tumor suppressor in neuroblastoma. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors become chromaffin cells of the adrenal gland. We …

0301 basic medicineTranscription GeneticCarcinogenesisChromaffin CellsRetinoic acidlaw.inventionNeuroblastomachemistry.chemical_compound0302 clinical medicinelawNerve Growth FactorMedicine and Health Sciencesretinoic acidAnaplastic Lymphoma Kinaselcsh:QH301-705.5NeuronsMice Inbred BALB CNeural crestCell DifferentiationPrognosisCandidate Tumor Suppressor GeneDLG2Up-RegulationCell biologyGene Expression Regulation NeoplasticERKPhenotypeTreatment Outcomemedicine.anatomical_structureFemaleChromosome Deletiontumor suppressorMAP Kinase Signaling SystemSp1 Transcription FactorSchwann cellGenetics and Molecular BiologyTretinoinBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAdrenergic AgentsCell Line TumorNeuroblastomamedicineAnimalsHumansProgenitor cellGenePsychological repressionCell ProliferationChromosomes Human Pair 11Tumor Suppressor Proteinsmedicine.disease030104 developmental biologyALKlcsh:Biology (General)chemistryTrk receptorGeneral BiochemistrySuppressorSchwann CellsGuanylate Kinases030217 neurology & neurosurgerySSRN Electronic Journal
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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)
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MiR-663, a MicroRNA Linked with Inflammation and Cancer That Is under the Influence of Resveratrol

2018

Resveratrol (trans-3,5,4′-trihydroxystilbene, RSV) is a non-flavonoid dietary polyphenol with antioxidant, anti-inflammatory and anti-cancer properties that is primarily found in red berries. While RSV displays many beneficial effects in vitro, its actual effects in vivo or in animal models remain passionately debated. Recent publications suggest that RSV pleiotropic effects could arise from its capability to regulate the expression and activity of microRNAs, short regulators themselves capable of regulating up to several hundreds of target genes. In particular, RSV increases microRNA miR-663 expression in different human cell lines, suggesting that at least some of its multiple benef…

0301 basic medicineTumor suppressor genelcsh:MedicineInflammationTumor initiationReviewResveratrolBiologyresveratrol03 medical and health scienceschemistry.chemical_compoundIn vivocardiovascular diseasemicroRNAmedicinecancerGeneGeneral Environmental Sciencelcsh:RGeneral EngineeringCancermedicine.diseasemiR-663030104 developmental biologychemistryinflammationCancer researchGeneral Earth and Planetary Sciencesmedicine.symptomMedicines
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Endogenous Myoglobin in Breast Cancer Is Hypoxia-inducible by Alternative Transcription and Functions to Impair Mitochondrial Activity

2011

Recently, immunohistochemical analysis of myoglobin (MB) in human breast cancer specimens has revealed a surprisingly widespread expression of MB in this nonmuscle context. The positive correlation with hypoxia-inducible factor 2α (HIF-2α) and carbonic anhydrase IX suggested that oxygen regulates myoglobin expression in breast carcinomas. Here, we report that MB mRNA and protein levels are robustly induced by prolonged hypoxia in breast cancer cell lines, in part via HIF-1/2-dependent transactivation. The hypoxia-induced MB mRNA originated from a novel alternative transcription start site 6 kb upstream of the ATG codon. MB regulation in normal and tumor tissue may thus be fundamentally diff…

0303 health sciencesGene knockdownTumor suppressor geneCell growthCellCell BiologyBiologyMitochondrionBiochemistryMolecular biology03 medical and health sciencesTransactivation0302 clinical medicinemedicine.anatomical_structure030220 oncology & carcinogenesisCancer cellmedicineCancer researchGene silencingMolecular Biology030304 developmental biologyJournal of Biological Chemistry
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