Search results for "small"

showing 10 items of 2441 documents

Aurora-A Transcriptional Silencing and Vincristine Treatment Show a Synergistic Effect in Human Tumor Cells

2008

Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G 2 /M cell cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide-, and paclitaxel-induced apoptosis.Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of hu…

Cancer ResearchPathologymedicine.medical_specialtyTranscription GeneticApoptosismacromolecular substancesProtein Serine-Threonine KinasesBiologyTransfectionPLK1Aurora KinasesRNA interferenceCell Line TumormedicineHumansGene silencingGene SilencingRNA Small InterferingMitotic catastropheCentrosomeCisplatinCarcinomaCell CycleDrug SynergismAuroraA/stk15centrosome amplificationAneuploidy CINGeneral MedicineCell cycleAneuploidyAntineoplastic Agents PhytogenicGene Expression Regulation NeoplasticSettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)OncologyVincristineCentrosomeColonic Neoplasmsembryonic structuresCancer cellCancer researchbiological phenomena cell phenomena and immunityHeLa Cellsmedicine.drugOncology Research Featuring Preclinical and Clinical Cancer Therapeutics
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Intestinal epithelial HuR modulates distinct pathways of proliferation and apoptosis and attenuates small intestinal and colonic tumor development.

2014

Abstract HuR is a ubiquitous nucleocytoplasmic RNA-binding protein that exerts pleiotropic effects on cell growth and tumorigenesis. In this study, we explored the impact of conditional, tissue-specific genetic deletion of HuR on intestinal growth and tumorigenesis in mice. Mice lacking intestinal expression of HuR (Hur IKO mice) displayed reduced levels of cell proliferation in the small intestine and increased sensitivity to doxorubicin-induced acute intestinal injury, as evidenced by decreased villus height and a compensatory shift in proliferating cells. In the context of Apcmin/+ mice, a transgenic model of intestinal tumorigenesis, intestinal deletion of the HuR gene caused a three-fo…

Cancer ResearchPost-translational regulationRNA-binding proteinContext (language use)ApoptosisCell Growth ProcessesBiologymedicine.disease_causeArticleAU-rich RNAMiceGene expressionIntestinal NeoplasmsmedicineAnimalsmRNA stabilityIntestinal MucosaMice KnockoutCell growthMolecular biologyPhenotypeProtein-RNA interactionSmall intestineDisease Models Animalmedicine.anatomical_structureOncologyELAV ProteinsApoptosisColonic NeoplasmsCancer researchCarcinogenesis
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Histone deacetylase inhibitors induce in human hepatoma HepG2 cells acetylation of p53 and histones in correlation with apoptotic effects

2007

This report shows that histone deacetylase inhibitors (HDACIs) induced apoptosis in human hepatoma HepG2 cells in a dose- and time-dependent manner. Trichostatin A (TSA), ITF2357 and suberoylanilide hydroxamic acid (SAHA), which were very effective agents, caused apoptotic effects after a lag phase of 12-16 h. In order to elucidate the mechanism of HDACIs action in HepG2 cells we have studied the effects of TSA, ITF2357 and SAHA on acetylation of p53 and histones H2A, H2B, H3 and H4. It was observed that HDACIs rapidly induced acetylation of these proteins, being the effects clearly visible already at 30 min of treatment at the same doses which caused apoptosis. Analysis of the immunocomple…

Cancer ResearchProgrammed cell deathCarcinoma Hepatocellularmedicine.drug_classAntineoplastic AgentsApoptosisBiologyHydroxamic AcidsHistonesCell Line TumorSettore BIO/10 - BiochimicamedicineHumansBenzothiazolesEnzyme InhibitorsRNA Small InterferingHistone AcetyltransferasesVorinostatHistone deacetylase inhibitors acetylation p53 histones apoptosis hepatoma cells.Liver NeoplasmsHistone deacetylase inhibitorAcetylationProto-Oncogene Proteins c-mdm2Molecular biologyHistone Deacetylase InhibitorsTrichostatin AHistoneOncologyPCAFAcetylationbiology.proteinHistone deacetylaseTumor Suppressor Protein p53DNA DamageToluenemedicine.drugInternational Journal of Oncology
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Differential Sensitivity of Malignant Glioma Cells to Methylating and Chloroethylating Anticancer Drugs: p53 Determines the Switch by Regulating xpc,…

2007

Abstract Glioblastoma multiforme is the most severe form of brain cancer. First line therapy includes the methylating agent temozolomide and/or the chloroethylating nitrosoureas [1-(2-chloroethyl)-1-nitrosourea; CNU] nimustine [1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea; ACNU], carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea; BCNU], or lomustine [1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea; CCNU]. The mechanism of cell death after CNU treatment is largely unknown. Here we show that ACNU and BCNU induce apoptosis in U87MG [p53 wild-type (p53wt)] and U138MG [p53 mutant (p53mt)] glioma cells. However, contrary to what we observed previously for temozolomide, chl…

Cancer ResearchProgrammed cell deathDNA repairAntineoplastic AgentsBiologychemistry.chemical_compoundCell Line TumorGliomamedicineHumansRNA NeoplasmRNA Small InterferingneoplasmsCarmustineTemozolomideBrain Neoplasmsorganic chemicalsNimustineDNA NeoplasmDNA Methylationmedicine.diseaseDNA-Binding ProteinsOncologychemistryCell cultureApoptosisCancer researchTumor Suppressor Protein p53GlioblastomaDNA Damagemedicine.drugCancer Research
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The plasma membrane channel ORAI1 mediates detrimental calcium influx caused by endogenous oxidative stress.

2013

The mouse hippocampal cell line HT22 is an excellent model for studying the consequences of endogenous oxidative stress. Addition of extracellular glutamate depletes the cells of glutathione (GSH) by blocking the glutamate-cystine antiporter system x(c)(-). GSH is the main antioxidant in neurons and its depletion induces a well-defined program of cell death called oxytosis, which is probably synonymous with the iron-dependent form of non-apoptotic cell death termed ferroptosis. Oxytosis is characterized by an increase of reactive oxygen species and a strong calcium influx preceding cell death. We found a significant reduction in store-operated calcium entry (SOCE) in glutamate-resistant HT2…

Cancer ResearchProgrammed cell deathORAI1 ProteinSTIM1AntiporterImmunologychemistry.chemical_elementApoptosisCalciumBiologymedicine.disease_causeAntioxidantsCell LineCellular and Molecular Neurosciencechemistry.chemical_compoundMicemedicineAnimalsStromal Interaction Molecule 1RNA Small InterferingStromal Interaction Molecule 2Calcium metabolismMembrane GlycoproteinsORAI1Cell MembraneCell BiologySTIM2GlutathioneGlutathioneCell biologyOxidative StresschemistryCalciumOriginal ArticleCalcium ChannelsReactive Oxygen SpeciesOxidative stressSOCECell deathdisease
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LS104, a non-ATP-competitive small-molecule inhibitor of JAK2, is potently inducing apoptosis in JAK2V617F-positive cells

2008

Abstract The activating JAK2V617F mutation has been described in the majority of patients with BCR-ABL-negative myeloproliferative disorders (MPD). In this report, we characterize the small-molecule LS104 as a novel non-ATP-competitive JAK2 inhibitor: Treatment of JAK2V617F-positive cells with LS104 resulted in dose-dependent induction of apoptosis and inhibition of JAK2 autophosphorylation and of downstream targets. Activation of these targets by JAK2 was confirmed in experiments using small interfering RNA. LS104 inhibited JAK2 kinase activity in vitro. This effect was not reversible using elevated ATP concentrations, whereas variation of the kinase substrate peptide led to modulation of …

Cancer ResearchSmall interfering RNAApoptosisStyrenesMiceAdenosine TriphosphateCell Line Tumorhemic and lymphatic diseasesAnimalsHumansPhosphorylationKinase activityProtein Kinase InhibitorsMyeloproliferative DisordersJanus kinase 2AcrylonitrileDose-Response Relationship DrugbiologyKinaseAutophosphorylationJanus Kinase 2Molecular biologyIn vitroOncologyApoptosisbiology.proteinSignal transductionK562 CellsSignal TransductionMolecular Cancer Therapeutics
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PO-053 The phospholipase ddhd1 as a new target in colorectal cancer therapy

2018

Introduction We have recently demonstrated that Citrus-limon derived nanovesicles are able to decrease colon cancer cell viability and that this effect is associated with the down-regulation of the intracellular phospholipase DDHD domain-containing protein 1 (DDHD1). While few studies are currently available on DDHD1 contribution in neurological disorders, information on its involvement in cancer is missing. Here we investigate the role of DDHD1 in colon cancer. Material and methods DDHD1 siRNAs and overexpression vector were transfected into colorectal cancer and normal cells to down-regulate or up-regulate DDHD1 expression. In vitro and in vivo assays were performed to investigate the fun…

Cancer ResearchSmall interfering RNAColorectal cancerCell growthCancerTransfectionBiologymedicine.diseaseOncologyCancer cellmedicineCancer researchGene silencingIntracellular
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MUC1 oncoprotein promotes refractoriness to chemotherapy in thyroid cancer cells.

2007

Abstract Overexpression of MUC1 oncoprotein is frequently observed in cancer and contributes to confer resistance to genotoxic agents. Papillary, follicular, and anaplastic thyroid carcinomas are the three forms of thyroid epithelial cancer. Anaplastic tumors are less differentiated and extremely aggressive, characterized by a poor prognosis. Little is known about the role of MUC1 in thyroid cancer. We recently showed that autocrine production of interleukin (IL)-4 and IL-10 controls thyroid cancer cell survival, growth, and resistance to chemotherapy through activation of Janus-activated kinase/signal transducers and activators of transcription (JAK/STAT) and phosphatidylinositide 3′-OH ki…

Cancer ResearchTranscription GeneticDrug ResistanceApoptosisSuppressor of Cytokine Signaling ProteinsnPhosphatidylinositol 3-KinasesAntibioticsMedicineRNA Small InterferingThyroid cancerTumorAntibiotics AntineoplasticThyroidAntineoplasticInterleukin-10Mitochondriamedicine.anatomical_structureOncologyTranscriptionSignal TransductionDown-RegulationSmall InterferingTransfectionCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinGeneticSettore MED/04 - PATOLOGIA GENERALEAntigens NeoplasmCell Line TumorHumansThyroid NeoplasmsAnaplastic thyroid cancerAntigensProtein kinase BPI3K/AKT/mTOR pathwayAntibiotics Antineoplastic; Antigens Neoplasm; Apoptosis; Cell Line Tumor; Down-Regulation; Doxorubicin; Drug Resistance Neoplasm; Humans; Interleukin-10; Interleukin-4; Mitochondria; Mucin-1; Mucins; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; RNA Small Interfering; Signal Transduction; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Transcription Genetic; Transfection; Cancer Research; Oncologybusiness.industryMucin-1MucinsCancermedicine.diseaseDoxorubicinDrug Resistance NeoplasmCancer cellCancer researchNeoplasmRNAInterleukin-4businessProto-Oncogene Proteins c-aktCancer research
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Abstract 2679: Virtual screening of small molecule inhibitors towards the tumor suppressor p53 to overcome radioresistance of nasopharyngeal carcinom…

2010

Abstract The tumor suppressor p53 belongs to the most frequently mutated genes in cancer, including nasopharyngeal carcinoma (NPC). p53 is over-expressed in NPC, but the mutation rate is lower than in other tumor types. Therefore, it can be hypothesized that p53 might be involved in repair of DNA-damage after radiotherapy and causes recrudescence. Hence, the aim of the present investigation was to identify small molecule inhibitors for p53 to inhibit DNA repair after ionizing radiation of NPC. Approximately 260.000 2D-structures from NCI database were downloaded and different tautomers and charged stages between pH 5 and 9 were calculated for each compound. A total number of 906.587 drugs i…

Cancer ResearchVirtual screeningChemistryDNA repairCancerAutoDockmedicine.diseaseBioinformaticsLigand (biochemistry)Small moleculeOncologyNasopharyngeal carcinomaRadioresistancemedicineCancer researchCancer Research
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Phase 0/1 of Positron Emission Tomography (PET) imaging agent [18F]-ODS2004436 as a marker of EGFR mutation in patients with non-small cell lung canc…

2018

e24184Background: Multiple EGFR tyrosine kinase inhibitors (TKIs) are approved for treatment of NSCLC harboring EGFR activating mutations or secondary TKIs resistant mutation. We evaluate a new PET...

Cancer Research[SDV.IB.IMA]Life Sciences [q-bio]/Bioengineering/Imagingnon-small cell lung cancer (NSCLC)[SDV.IB.MN]Life Sciences [q-bio]/Bioengineering/Nuclear medicine[SDV.IB.MN] Life Sciences [q-bio]/Bioengineering/Nuclear medicine03 medical and health sciences0302 clinical medicinemedicineIn patientComputingMilieux_MISCELLANEOUSmedicine.diagnostic_testbusiness.industryPet imagingmedicine.diseaseEGFR Tyrosine Kinase Inhibitorsrespiratory tract diseases3. Good health[SDV.IB.IMA] Life Sciences [q-bio]/Bioengineering/ImagingOncologyEgfr mutationPositron emission tomography030220 oncology & carcinogenesisMutation (genetic algorithm)Cancer researchbusiness030215 immunology
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