Search results for " Neoplastic"

showing 10 items of 662 documents

Induction of cholesterol biosynthesis by archazolid B in T24 bladder cancer cells.

2014

Abstract Background Resistance of cancer cells towards chemotherapeutics represents a major cause of therapy failure. The objective of our study was to evaluate cellular defense strategies in response to the novel vacuolar H+-ATPase inhibitor, archazolid B. Experimental approach: The effects of archazolid B on T24 bladder carcinoma cells were investigated by combining “omics” technologies (transcriptomics (mRNA and miRNA) and proteomics). Free cholesterol distribution was determined by filipin staining using flow cytometry and fluorescence microscopy. Flow cytometry was performed for LDLR surface expression studies. Uptake of LDL cholesterol was visualized by confocal microscopy. SREBP acti…

IndolesCell SurvivalBiologyReal-Time Polymerase Chain ReactionBiochemistryFatty Acids Monounsaturatedchemistry.chemical_compoundCell Line TumormedicineHumansFluvastatinPharmacologyCholesterolReproducibility of ResultsMolecular biologySterolEndocytosisSterol regulatory element-binding proteinGene Expression Regulation NeoplasticLipoproteins LDLMicroRNAsThiazolesCell killingCholesterolchemistryReceptors LDLUrinary Bladder NeoplasmsDrug Resistance NeoplasmLDL receptorCancer celllipids (amino acids peptides and proteins)Sterol regulatory element-binding protein 2MacrolidesSterol Regulatory Element Binding Protein 1Fluvastatinmedicine.drugSterol Regulatory Element Binding Protein 2Biochemical pharmacology
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Endometrial receptivity and implantation are not affected by the presence of uterine intramural leiomyomas: a clinical and functional genomics analys…

2008

Uterine leiomyomas are the most frequent benign tumors during reproductive age. Whether intramural leiomyomas cause infertility and should be removed is controversial because no study has addressed the underlying mechanism of infertility.The objective of the study was to test the effect of intramural leiomyomas on endometrial function by comparing gene during the window of implantation and implantation in an oocyte donation program, in which the quality of the embryos replaced is similar and the endocrine environment of the endometrium is standardized by exogenous steroids.Human endometria of women with single intramural leiomyomas (group A,5 cm and group B,or =5 cm) and controls (group C) …

InfertilityAdultmedicine.medical_specialtyPregnancy RateEndocrinology Diabetes and Metabolismmedicine.medical_treatmentClinical BiochemistryUterusContext (language use)BiologyEndometriumBiochemistryModels BiologicalEndometriumEndocrinologyPregnancyInternal medicinemedicineCluster AnalysisHumansEmbryo ImplantationOligonucleotide Array Sequence AnalysisRetrospective StudiesGynecologyIn vitro fertilisationUterine leiomyomaLeiomyomaGene Expression ProfilingBiochemistry (medical)GenomicsMiddle Agedmedicine.diseaseGene Expression Regulation NeoplasticPregnancy ratemedicine.anatomical_structureEndocrinologyIn uteroUterine NeoplasmsFemalePregnancy Complications NeoplasticThe Journal of clinical endocrinology and metabolism
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The inhibitor of differentiation-1 (Id1) enables lung cancer liver colonization through activation of an EMT program in tumor cells and establishment…

2017

Abstract: Id1 promotes carcinogenesis and metastasis, and predicts prognosis of non-small cell lung cancer (NSCLC)-adenocarcionoma patients. We hypothesized that Id1 may play a critical role in lung cancer colonization of the liver by affecting both tumor cells and the microenvironment. Depleted levels of Id1 in LLC (Lewis lung carcinoma cells, LLC shId1) significantly reduced cell proliferation and migration in vitro. Genetic loss of Id1 in the host tissue (Id1(-/-) mice) impaired liver colonization and increased survival of Id1 animals. Histologically, the presence of Idl in tumor cells of liver metastasis was responsible for liver colonization. Microarray analysis comparing liver tumor n…

Inhibitor of Differentiation Protein 10301 basic medicineCancer ResearchPathologyLung NeoplasmsTime Factors10255 Clinic for Thoracic SurgeryVimentinmedicine.disease_causeMetastasisCarcinoma Lewis Lung0302 clinical medicineCell MovementCarcinoma Non-Small-Cell LungTumor Microenvironment1306 Cancer ResearchMice KnockoutTissue microarrayIntegrin beta1Liver NeoplasmsTumor BurdenGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesis2730 OncologySignal Transductionmedicine.medical_specialtyEpithelial-Mesenchymal TransitionLiver tumor610 Medicine & healthBiologyTransforming Growth Factor beta103 medical and health sciencesCell Line Tumor10049 Institute of Pathology and Molecular PathologymedicineAnimalsHumansVimentinEpithelial–mesenchymal transitionLung cancerCell ProliferationLewis lung carcinomamedicine.diseaseMice Inbred C57BL030104 developmental biologyCancer researchbiology.proteinHuman medicineSnail Family Transcription FactorsCarcinogenesisCancer Letters
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Pro-prion Binds Filamin A, Facilitating Its Interaction with Integrin β1, and Contributes to Melanomagenesis

2010

Filamin A (FLNA) is an integrator of cell mechanics and signaling. The spreading and migration observed in FLNA sufficient A7 melanoma cells but not in the parental FLNA deficient M2 cells have been attributed to FLNA. In A7 and M2 cells, the normal prion (PrP) exists as pro-PrP, retaining its glycosylphosphatidyl-inositol (GPI) anchor peptide signal sequence (GPI-PSS). The GPI-PSS of PrP has a FLNA binding motif and binds FLNA. Reducing PrP expression in A7 cells alters the spatial distribution of FLNA and organization of actin and diminishes cell spreading and migration. Integrin β1 also binds FLNA. In A7 cells, FLNA, PrP, and integrin β1 exist as two independent, yet functionally linked,…

Integrin beta ChainsGlycosylphosphatidylinositolsPrionsFilaminsanimal diseasesAmino Acid MotifsIntegrinPlasma protein bindingBiologyFilaminBiochemistryCell membraneContractile ProteinsCell MovementCell Line TumormedicineHumansFLNACytoskeletonMelanomaMolecular BiologyActinMicrofilament ProteinsCell Biologynervous system diseasesCell biologyGene Expression Regulation Neoplasticmedicine.anatomical_structurebiology.proteinCancer researchSignal transductionProtein BindingJournal of Biological Chemistry
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The Selective Regulation of αVβ1 Integrin Expression Is Based on the Hierarchical Formation of αV-containing Heterodimers

2002

The integrin beta1 subunit can form a heterodimer with 12 different alpha subunits. According to the present model, the expression level of any alphabeta complex is regulated by the availability of the specific alpha subunit, whereas beta1 subunit is constantly present in a large excess. The expression of several heterodimers containing the alphaV subunit seems to be regulated by an identical mechanism. The fact that many cells express alphaVbeta1 heterodimer, and that this fibronectin/vitronectin receptor may be selectively regulated, compromises the present model of the regulation of beta1 and alphaV integrins. We have tried to solve this problem by assuming that distinct alphabeta hetero…

IntegrinsProtein subunitCellIntegrinBiologyModels BiologicalBiochemistryAntigens CDComplementary DNATumor Cells CulturedmedicineHumansReceptors VitronectinMelanomaMolecular BiologyCell MembraneCell BiologyTransfectionIntegrin alphaVFibronectinsCell biologyGene Expression Regulation NeoplasticFibronectinmedicine.anatomical_structurebiology.proteinVitronectinCollagenDimerizationIntracellularProtein BindingJournal of Biological Chemistry
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Induction of interferon regulatory factors, 2′‐5′ oligoadenylate synthetase, P68 kinase and RNase L in chronic myelogenous leukaemia cells and its re…

1996

The genes crucially determining the therapeutic response of chronic myelogenous leukaemia (CML) to interferon-alpha (IFN-alpha) are unknown. Recently, two independent IFN-alpha signalling pathways were identified: the classic pathway mediates induction of 2'-5' oligoadenylate synthetase (2-5 OAS), p68 kinase and IFN regulatory factor-2 (IRF-2), whereas the alternate pathway leads to activation of IFN regulatory factor-1 (IRF-1). We investigated whether deficient or imbalanced expression of components of these two pathways is associated with resistance of CML cells to antiproliferative action of IFN alpha/beta. Constitutive and IFN-induced transcript levels of IFN-dependent genes in mononucl…

Interferon Regulatory Factor 2T-LymphocytesCellular differentiationmedicine.medical_treatmentProtein Serine-Threonine KinaseseIF-2 KinaseLeukemia Myelogenous Chronic BCR-ABL PositiveEndoribonucleases2'5'-Oligoadenylate SynthetasemedicineHumansRNA MessengerTreatment FailureInterferon alfaEIF-2 kinasebiology2'-5'-OligoadenylateInterferon-alphaHematologyBlotting NorthernHematopoietic Stem CellsPhosphoproteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsCytokineIRF1Cancer researchbiology.proteinInterferon Regulatory Factor-2GranulocytesInterferon Regulatory Factor-1Transcription Factorsmedicine.drugInterferon regulatory factorsBritish Journal of Haematology
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Artemisinin derivatives induce iron-dependent cell death (ferroptosis) in tumor cells

2015

Abstract Background Apoptosis and other forms of cell death have been intensively investigated in the past years to explain the mode of action of synthetic anticancer drugs and natural products. Recently, a new form of cell death emerged, which was termed ferroptosis, because it depends on intracellular iron. Here, the role of genes involved in iron metabolism and homeostasis for the cytotoxicity of ten artemisinin derivatives have been systematically investigated. Material and methods Log10IC50 values of 10 artemisinin derivatives (artesunate, artemether, arteether, artenimol, artemisitene, arteanuin B, another monomeric artemisinin derivative and three artemisinin dimer molecules) were co…

IronArtesunatePharmaceutical ScienceApoptosisTransferrin receptorDeferoxaminePhenylenediaminesPharmacologyBiologyInhibitory Concentration 50chemistry.chemical_compoundCell Line Tumorparasitic diseasesDrug DiscoverymedicineHumansArtemetherArtemisininCytotoxicityOligonucleotide Array Sequence AnalysisPharmacologychemistry.chemical_classificationCyclohexylaminesCell DeathMolecular StructureArtemisinin DimerArtemisininsGene Expression Regulation NeoplasticComplementary and alternative medicinechemistryApoptosisTransferrinArtesunateMolecular MedicineArtemethermedicine.drugPhytomedicine
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Cigarette smoke affects the onco-suppressor DAB2IP expression in bronchial epithelial cells of COPD patients

2019

AbstractCigarette smoke is a risk factor for COPD and lung cancer. In cancer, epigenetic modifications affect the expression of Enhancer of Zester Homolog 2 (EZH2), and silenced disabled homolog 2 interacting protein gene (DAB2IP) (onco-suppressor gene) by Histone H3 tri-methylation in lysine 27 (H3K27me3). In“ex vivo”studies, we assessed EZH2, H3K27me3 and DAB2IP immunoreactivity in bronchial epithelial cells from COPD patients (smokers, ex-smokers), Smoker and control subjects. In“in vitro” experiments we studied the effect of cigarette smoke extract (CSE) on EZH2/H3K27me3/DAB2IP expression, apoptosis, invasiveness, and vimentin expression in 16HBE, primary cells, and lung cancer cell lin…

Jumonji Domain-Containing Histone DemethylasesLung NeoplasmsCigar SmokingCelllcsh:MedicineApoptosismacromolecular substancesArticlePulmonary Disease Chronic ObstructiveRisk FactorsmedicineHumansEnhancer of Zeste Homolog 2 ProteinNeoplasm Invasivenesslcsh:ScienceLung cancerA549 CellOncogenesisInflammationA549 cellRegulation of gene expressionCOPDMultidisciplinarybusiness.industrylcsh:REZH2ApoptosiJumonji Domain-Containing Histone DemethylaseCancerras GTPase-Activating Proteinmedicine.diseaseAlveolar Epithelial Cellrespiratory tract diseasesLung NeoplasmGene Expression Regulation NeoplasticNeoplasm Invasiveness Pulmonary Disease Chronic Obstructivemedicine.anatomical_structureA549 Cellsras GTPase-Activating ProteinsApoptosisAlveolar Epithelial CellsCancer researchlcsh:QbusinessHumanairway disease
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Telomerase Reverse Transcriptase Delays Aging in Cancer-Resistant Mice

2008

Summary Telomerase confers limitless proliferative potential to most human cells through its ability to elongate telomeres, the natural ends of chromosomes, which otherwise would undergo progressive attrition and eventually compromise cell viability. However, the role of telomerase in organismal aging has remained unaddressed, in part because of the cancer-promoting activity of telomerase. To circumvent this problem, we have constitutively expressed telomerase reverse transcriptase (TERT), one of the components of telomerase, in mice engineered to be cancer resistant by means of enhanced expression of the tumor suppressors p53, p16, and p19ARF. In this context, TERT overexpression improves …

KeratinocytesAgingTelomeraseCell SurvivalTransgeneHUMDISEASEMice TransgenicContext (language use)BiologyModels BiologicalGene Expression Regulation EnzymologicGeneral Biochemistry Genetics and Molecular BiologyMiceNeoplasmsmedicineAnimalsHumansTelomerase reverse transcriptaseViability assayInsulin-Like Growth Factor ITelomeraseRegulation of gene expressionBiochemistry Genetics and Molecular Biology(all)Stem CellsCancermedicine.diseaseMolecular biologyTelomereGene Expression Regulation NeoplasticCancer researchCELLBIOEpidermisCell
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An integrated humoral and cellular response is elicited in pancreatic cancer by alpha-enolase, a novel pancreatic ductal adenocarcinoma-associated an…

2009

Pancreatic ductal adenocarcinoma (PDAC) is a fatal disease with a very poor 5-year survival rate. alpha-Enolase is a glycolytic enzyme that also acts as a surface plasminogen receptor. We find that it is overexpressed in PDAC and present on the cell surface of PDAC cell lines. The clinical correlation of its expression with tumor status has been reported for lung and hepatocellular carcinoma. We have previously demonstrated that sera from PDAC patients contain IgG autoantibodies to alpha-enolase. The present work was intended to assess the ability of alpha-enolase to induce antigen-specific T cell responses. We show that alpha-enolase-pulsed dendritic cells (DC) specifically stimulate healt…

KeratinocytesCancer ResearchPancreatic diseaseendocrine system diseasesalpha-enolaseAntibodies NeoplasmAlpha-enolaseT-LymphocytesMiceSkinImmunity Cellularhuman; pancreatic ductal adenocarcinoma; alpha enolase; tumor antigen; B cell response; T cell responsebiologyalpha enolasehuman; pancreatic ductal adenocarcinoma; alpha-enolase; tumor antigen; B cell response; T cell responseImmunohistochemistryTumor antigenUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyAntibodyCarcinoma Pancreatic DuctalB cell responseT cellBlotting Westernpancreatic ductal adenocarcinomaGene Expression Regulation EnzymologicInterferon-gammaImmune systemAntigenAntigens NeoplasmCell Line TumorPancreatic cancermedicineAnimalsHumanshumanPancreasCell ProliferationDendritic Cellsmedicine.diseaseT cell responsepancreatic ductal adenocarcinoma; alpha-enolase; tumor antigen.digestive system diseasesPancreatic NeoplasmsImmunoglobulin GPhosphopyruvate HydrataseAntibody FormationImmunologybiology.proteintumor antigenT-Lymphocytes Cytotoxic
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