Search results for "expression"

showing 10 items of 5168 documents

Immune escape of AKT overexpressing ovarian cancer cells

2012

Platinum-resistance is the most crucial problem for treatment of ovarian cancer. There is a clinical need for new treatment strategies which overcome platinum resistance. As survival is strongly influenced by immunological parameters, immunotherapeutic strategies appear promising. Therefore a better understanding of the interaction between ovarian tumour cells and cells of the immune system is a necessary prerequisite. In the present study we aimed to enlighten the interactions between platinum resistant and platinum sensitive ovarian cancer cells and natural-killer (NK)-cells. Modified FATAL assay was used for determining the killing efficiency of NK-cells for the parental A2780 cells and …

Cancer Researchendocrine system diseasesUbiquitin-Protein LigasesCellApoptosisBiologymedicine.disease_causeInhibitor of Apoptosis ProteinsImmune systemCell Line TumormedicineHumansPlatinumOvarian NeoplasmsCancerCell cyclemedicine.diseaseBaculoviral IAP Repeat-Containing 3 Proteinfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticKiller Cells Naturalmedicine.anatomical_structureOncologyDrug Resistance NeoplasmCell cultureApoptosisCancer researchFemaleOvarian cancerCarcinogenesisProto-Oncogene Proteins c-aktInternational Journal of Oncology
researchProduct

Histone deacetylase inhibitors: apoptotic effects and clinical implications (Review).

2008

It has been shown that epigenetic modifications play an important role in tumorigenesis. Thus, affecting epigenetic tumorigenic alterations can represent a promising strategy for anticancer targeted therapy. Among the key chromatin modifying enzymes which influence gene expression, histone acetyltransferases (HATs) and histone deacetylases (HDACs) have recently attracted interest because of their impact on tumor development and progression. Increased expression of HDACs and disrupted activities of HATs have been found in several tumor types, with a consequent hypoacetylated state of chromatin that can be strictly correlated with low expression of either tumor suppressor or pro-apoptotic gen…

Cancer Researchmedicine.drug_classAntineoplastic AgentsApoptosisBiologyHydroxamic AcidsModels BiologicalRomidepsinEpigenesis Geneticchemistry.chemical_compoundDepsipeptidesNeoplasmsSettore BIO/10 - BiochimicamedicineHumansEpigeneticsVorinostatSulfonamidesVorinostatHistone deacetylase inhibitorHDACI apoptosisChromatinChromatinProtein Structure TertiaryGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsHistoneOncologychemistryModels ChemicalCancer researchbiology.proteinHistone deacetylaseBelinostatmedicine.drug
researchProduct

Resistance factors in colon cancer tissue and the adjacent normal colon tissue: glutathione S-transferases alpha and pi, glutathione and aldehyde deh…

1998

Abstract Glutathione S -transferases (GST) α and π , glutathione (GSH) and aldehyde dehydrogenase (ADH) were determined in colorectal cancer tissue specimens and in the adjacent normal colon tissue. The median contents in normal and cancer tissue were 8.1 (2.3–30.3) (5–95% quantiles) and 15.1 (5.3–50.3) μ g/mg protein for GST π ( P =0.035), 0.0 (0.0–1.4) and 0.4 (0.0–3.5) μ g/mg protein for GST α ( P =0.019), 7.3 (1.3–22.7) and 5.6 (2.3–26.0) μ g/mg protein for GSH ( P =0.171) and 30.8 (13.0–42.0) and 23.2 (9.0–32.9) μ g/mg protein for ADH ( P =0.0017), respectively. Thus, the mean GST α and π both significantly increased in colon cancer compared to the adjacent normal tissue, which underli…

Cancer Researchmedicine.medical_specialtyColorectal cancerColonAldehyde dehydrogenaseBiologymedicine.disease_causeIsozymeGene productchemistry.chemical_compoundInternal medicineGene expressionmedicineHumansGlutathione TransferaseCancerGlutathioneAldehyde Dehydrogenasemedicine.diseaseGlutathioneEndocrinologyOncologychemistryDrug Resistance NeoplasmColonic Neoplasmsbiology.proteinCarcinogenesisCancer letters
researchProduct

aPKCζ cortical loading is associated with Lgl cytoplasmic release and tumor growth in Drosophila and human epithelia

2007

Atypical protein kinase C (aPKC) and Lethal giant larvae (Lgl) regulate apical-basal polarity in Drosophila and mammalian epithelia. At the apical domain, aPKC phosphorylates and displaces Lgl that, in turn, maintains aPKC inactive at the basolateral region. The mutual exclusion of these two proteins seems to be crucial for the correct epithelial structure and function. Here we show that a cortical aPKC loading induces Lgl cytoplasmic release and massive overgrowth in Drosophila imaginal epithelia, whereas a cytoplasmic expression does not alter proliferation and epithelial overall structure. As two aPKC isoforms (iota and zeta) exist in humans and we previously showed that Drosophila Lgl i…

Cancer Researchmedicine.medical_specialtyCytoplasmAPKCz; Cell polarity; Drosophila; Hugl-1; Lethal giant larvae; Ovarian epithelial cancersAPKCzEpitheliumInternal medicineDrosophilidaeCell polarityGeneticsmedicineAnimalsDrosophila ProteinsHumansWings AnimalMolecular BiologyProtein kinase CProtein Kinase CCell ProliferationRegulation of gene expressionOvarian NeoplasmsbiologyTumor Suppressor ProteinsGene Expression Regulation DevelopmentalHugl-1Lethal giant larvaebiology.organism_classificationProtein subcellular localization predictionEpitheliumOvarian epithelial cancersCell biologyEndocrinologymedicine.anatomical_structureDrosophila melanogasterPhenotypeGene Expression RegulationCell polarityFemaleDrosophilaDrosophila melanogasterDrosophila Protein
researchProduct

Genome-Wide Haplotype Analysis of Cis Expression Quantitative Trait Loci in Monocytes

2013

In order to assess whether gene expression variability could be influenced by several SNPs acting in cis, either through additive or more complex haplotype effects, a systematic genome-wide search for cis haplotype expression quantitative trait loci (eQTL) was conducted in a sample of 758 individuals, part of the Cardiogenics Transcriptomic Study, for which genome-wide monocyte expression and GWAS data were available. 19,805 RNA probes were assessed for cis haplotypic regulation through investigation of ∼2,1×109 haplotypic combinations. 2,650 probes demonstrated haplotypic p-values >104-fold smaller than the best single SNP p-value. Replication of significant haplotype effects were tested f…

Cancer Researchmedicine.medical_specialtyHereditylcsh:QH426-470Immune Cells[SDV]Life Sciences [q-bio]Quantitative Trait LociImmunologyGene ExpressionGenome-wide association studySingle-nucleotide polymorphismQuantitative trait locusBiologyRegulatory Sequences Nucleic AcidPolymorphism Single NucleotideMonocytes03 medical and health sciences0302 clinical medicineMolecular geneticsmedicineGeneticsGenome-Wide Association StudiesSNPHumansGenetic Predisposition to DiseaseMolecular BiologyBiologyGenetics (clinical)Ecology Evolution Behavior and Systematics030304 developmental biologyGenetics0303 health sciencesQuantitative TraitsComplex TraitsHaplotypeGenomicslcsh:GeneticsGene Expression RegulationHaplotypesExpression quantitative trait lociGenome Expression Analysis030217 neurology & neurosurgeryImputation (genetics)Population GeneticsGenome-Wide Association StudyResearch Article
researchProduct

Hypoxia-induced epithelial VEGF-C/VEGFR-3 upregulation in carcinoma cell lines

2008

Adaptation to hypoxia, a universal hallmark of carcinomas, is a critical step for tumor cell survival and growth. One of the principal regulators of hypoxia-responsive pathways is the transcription factor hypoxia-inducible factor-1 alpha (HIF-1 alpha). Currently, it is known that tumoral production of members of the vascular endothelial growth factor (VEGF)-family (VEGFs) may promote tumor growth and progression by acting on carcinoma cells that express the cognate receptors (VEGFRs). However, the influence of hypoxia in the formation of such a tumoral VEGF/VEGFR loop is not completely understood. In the present study we examined the potential existence of a HIF-1 alpha/VEGF/VEGFR autocrine…

Cancer Researchmedicine.medical_specialtyLung NeoplasmsVascular Endothelial Growth Factor CCellBreast NeoplasmsBiologychemistry.chemical_compoundDownregulation and upregulationCell Line TumorInternal medicinemedicineHumansAutocrine signallingVascular Endothelial Growth Factor Receptor-1CarcinomaKinase insert domain receptorCell cycleHypoxia-Inducible Factor 1 alpha SubunitVascular Endothelial Growth Factor Receptor-3Vascular Endothelial Growth Factor Receptor-2Cell HypoxiaUp-RegulationGene Expression Regulation NeoplasticVascular endothelial growth factorAutocrine CommunicationHIF1AEndocrinologymedicine.anatomical_structureOncologyVascular endothelial growth factor CchemistryCancer researchColorectal NeoplasmsInternational Journal of Oncology
researchProduct

Transforming growth factor-β1, β2, and β3, urokinase and parathyroid hormone-related peptide expression in 8701-BC breast cancer cells and clones

1993

8701-BC is a recently characterized cell line isolated from a primary ductal infiltrating carcinoma of the breast (d.i.c.), showing some pleomorphism in cell microanatomy at an ultrastructural level. We have obtained different sublines of 8701-BC cells by cloning in soft agar at different concentrations (0.3% and 0.6%), and we have characterized the cloned lines by some morphological and growth parameters. 8701-BC cells and clones have been submitted to analysis by reverse transcriptase-linked polymerase chain reaction to detect mRNAs of various cytokines (transforming growth factor-beta s, tumour necrosis factors, interleukin 1s, interleukin 6, parathyroid hormone-related peptide, gamma in…

Cancer Researchmedicine.medical_specialtyMolecular Sequence DataParathyroid hormoneBreast NeoplasmsPolymerase Chain ReactionTransforming Growth Factor betaInternal medicineGene expressionBiomarkers TumorTumor Cells CulturedmedicineHumansRNA MessengerMolecular BiologyBase SequencebiologyParathyroid hormone-related proteinInterleukin-6Tumor Necrosis Factor-alphaCarcinoma Ductal BreastParathyroid Hormone-Related ProteinProteinsInterleukinCell BiologyTransforming growth factor betaUrokinase-Type Plasminogen ActivatorMolecular biologyIn vitroClone CellsPhenotypeEndocrinologyCell culturebiology.proteinInterleukin-1Developmental BiologyTransforming growth factorDifferentiation
researchProduct

Regulation of endothelial-type NO synthase expression in pathophysiology and in response to drugs.

2002

In many types of cardiovascular pathophysiology such as hypercholesterolemia and atherosclerosis, diabetes, cigarette smoking, or hypertension (with its sequelae stroke and heart failure) the expression of endothelial NO synthase (eNOS) is altered. Both up- and downregulation of eNOS have been observed, depending on the underlying disease. When eNOS is upregulated, the upregulation is often futile and goes along with a reduction in bioactive NO. This is due to an increased production of superoxide generated by NAD(P)H oxidase and by an uncoupled eNOS. A number of drugs with favorable effects on cardiovascular disease upregulate eNOS expression. The resulting increase in vascular NO producti…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryPharmacologymedicine.disease_causeNitric OxideBiochemistrychemistry.chemical_compoundDownregulation and upregulationMetabolic DiseasesEnosInternal medicineDiabetes mellitusmedicineAnimalsHumansEndothelial dysfunctionAngiotensin II receptor type 1biologybusiness.industrySuperoxidemedicine.diseasebiology.organism_classificationEndocrinologychemistryGene Expression RegulationErythropoietinCardiovascular DiseasesNitric Oxide SynthasebusinessOxidative stressmedicine.drugNitric oxide : biology and chemistry
researchProduct

Physiological mechanisms regulating the expression of endothelial-type NO synthase

2002

Although endothelial nitric oxide synthase (eNOS) is a constitutively expressed enzyme, its expression is regulated by a number of biophysical, biochemical, and hormonal stimuli, both under physiological conditions and in pathology. This review summarizes the recent findings in this field. Shear stress, growth factors (such as transforming growth factor-beta, fibroblast growth factor, vascular endothelial growth factor, and platelet-derived growth factor), hormones (such as estrogens, insulin, angiotensin II, and endothelin 1), and other compounds (such as lysophosphatidylcholine) upregulate eNOS expression. On the other hand, the cytokine tumor necrosis factor-alpha and bacterial lipopolys…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyRNA Stabilitymedicine.medical_treatmentClinical BiochemistryBiologyFibroblast growth factorBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundEnosInternal medicinemedicineAnimalsPromoter Regions GeneticRegulation of gene expressionBase SequenceGene Expression ProfilingGrowth factorbiology.organism_classificationActin cytoskeletonAngiotensin IICell biologyVascular endothelial growth factorEndocrinologychemistryNitric Oxide SynthaseSignal transductionSignal TransductionNitric Oxide
researchProduct

GADD45α is highly expressed in pancreatic ductal adenocarcinoma cells and required for tumor cell viability

2005

Pancreatic ductal adenocarcinoma is one of the most common causes of cancer death in the western civilization. Recently, NF-kappaB has been shown to be activated in pancreatic ductal adenocarcinoma through constitutive activation of IkappaB kinase (IKK). Inhibition of NF-kappaB by a super-inhibitor of NF-kappaB--delta-N-IkappaBalpha--resulted in impaired proliferation and induction of apoptosis, suggesting an important role of NF-kappaB in pancreatic tumorigenesis. Downstream target genes of IkappaBalpha have not been elucidated in pancreatic ductal adenocarcinoma in detail. Using expression profiling by cDNA array analysis of pancreatic ductal adenocarcinoma cell lines stably transfected w…

Cancer Researchmedicine.medical_specialtyPancreatic diseaseCell SurvivalDown-RegulationCell Cycle ProteinsIκB kinaseAdenocarcinomaBiologymedicine.disease_causeDownregulation and upregulationPancreatic cancerInternal medicinemedicineHumansCell ProliferationCell growthGene Expression ProfilingNF-kappa BNuclear Proteinsmedicine.diseaseI-kappa B KinasePancreatic NeoplasmsEndocrinologyOncologyApoptosisCancer researchRNA InterferenceCA19-9CarcinogenesisCarcinoma Pancreatic DuctalInternational Journal of Cancer
researchProduct