Search results for "TUMOR CELLS"

showing 10 items of 663 documents

Swelling of glial cells in lactacidosis and by glutamate: significance of Cl(-)-transport.

1993

Swelling of glial and nerve cells is characteristic of brain damage in cerebral ischemia or trauma. The therapeutical efficiency of inhibition of Cl(-)-transport by a novel antagonist, the diuretic torasemide, on cytotoxic swelling of glial cells from lactacidosis, or glutamate was analyzed. Lactacidosis and the interstitial accumulation of glutamate are hallmarks of the pathophysiological alterations in ischemic or traumatic brain tissue. C6 glioma cells harvested from culture and suspended in a physiological medium were either exposed to pH 6.2, or 5.0 by lactic acid, or exposed to 1 mM glutamate at normal pH. Cell swelling and viability were quantified by flow cytometry. Lactacidosis of …

IschemiaGlutamic AcidBrain EdemaPharmacologyIon Channelschemistry.chemical_compoundChloridesGlutamatesChloride ChannelsmedicineTumor Cells CulturedAnimalsDiureticsMolecular BiologyAcidosisCell SizeSulfonamidesIon TransportChemistryGeneral NeuroscienceGlutamate receptorMembrane ProteinsGlutamic acidmedicine.diseaseTorsemideLactic acidRatsmedicine.anatomical_structureBiochemistryCell cultureNeurogliaAcidosis LacticNeurology (clinical)Swellingmedicine.symptomNeurogliaDevelopmental BiologyBrain research
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The cell adhesion domain of type XVII collagen promotes integrin-mediated cell spreading by a novel mechanism.

2001

Type XVII collagen (BP180) is a keratinocyte transmembrane protein that exists as the full-length protein in hemidesmosomes and as a 120-kDa shed ectodomain in the extracellular matrix. The largest collagenous domain of type XVII collagen, COL15, has been described previously as a cell adhesion domain (Tasanen, K., Eble, J. A., Aumailley, M., Schumann, H., Baetge, J, Tu, H., Bruckner, P., and Bruckner-Tuderman, L. (2000) J. Biol. Chem. 275, 3093-3099). In the present work, the integrin binding of triple helical, human recombinant COL15 was tested. Solid phase binding assays using recombinant integrin alpha(1)I, alpha(2)I, and alpha(10)I domains and cell spreading assays with alpha(1)beta(1)…

KeratinocytesIntegrinsDNA ComplementaryDystoninIntegrinAmino Acid MotifsNerve Tissue ProteinsCHO CellsBiochemistryAutoantigensCollagen receptorCell LineCell MovementCricetinaeCell AdhesionTumor Cells CulturedAnimalsHumansCloning MolecularCell adhesionMolecular BiologyIntegrin bindingbiologyDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionHemidesmosomeCell BiologyNon-Fibrillar CollagensMolecular biologyRecombinant ProteinsProtein Structure TertiaryFibronectinHaCaTCytoskeletal ProteinsEctodomainbiology.proteinCollagenCarrier ProteinsPeptidesProtein BindingThe Journal of biological chemistry
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In contrast to their murine counterparts, normal human keratinocytes and human epidermoid cell lines A431 and HaCaT fail to express IL-10 mRNA and pr…

1997

Abstract In mice, keratinocyte-derived IL-10 is up-regulated by ultraviolet-B (UVB) radiation and plays a major role in UVB-induced immunosuppression. The present study was designed to examine whether a comparable phenomenon can be detected in man. Freshly isolated or cultured normal human keratinocytes (NHK) and keratinocyte cell lines A431 and HaCaT were stimulated with graded doses of UVB (up to 200 J/m2) or with a variety of other stimuli. RNA was extracted at various time points post-stimulation and analysed by reverse transcriptase-polymerase chain reaction (RT-PCR) using four different IL-10-specific primer pairs and RNA from monocytes or T cells as positive controls. We failed to de…

KeratinocytesMaleCell typeUltraviolet Raysmedicine.medical_treatmentImmunologyBiologyMelanocyteEpitheliumMicemedicineTumor Cells CulturedImmunology and AllergyAnimalsHumansRNA MessengerMessenger RNAEpidermis (botany)integumentary systemOriginal ArticlesInterleukin-10HaCaTCytokinemedicine.anatomical_structureCell cultureImmunologyMelanocytesKeratinocyteClinical and experimental immunology
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Cytotoxic Activity of Some Natural and Synthetic ent-Kauranes

2007

Atractyligenin (1) and several synthetic derivatives were tested and found to be active against tumor cell replication. Compound 1 was readily converted to the 2,15-diketo (3) or 15-keto (4) derivatives, which contain an alpha,beta-unsaturated ketone. Compounds 3 and 4 showed significant cytotoxic activity against all six tested cancer cell lines and were most potent against 1A9 ovarian cancer cells with EC50 values of 0.2 and 0.3 microM, respectively. These two 1-analogues are promising lead compounds for further investigation.

KetoneStereochemistryPharmaceutical ScienceAsteraceaeAtractylosideBiologyANTITUMOR AGENTSAnalytical Chemistrychemistry.chemical_compoundDrug DiscoveryTumor Cells CulturedHumansCytotoxic T cellCytotoxicityOvarian NeoplasmsPharmacologychemistry.chemical_classificationLamiaceaePlants MedicinalMolecular StructureDERIVATIVESOrganic ChemistryBiological activityAntineoplastic Agents PhytogenicTerpenoidIn vitroComplementary and alternative medicinechemistryBiochemistryCell cultureMolecular MedicineFemaleDrug Screening Assays AntitumorDiterpeneDiterpenes KauraneJournal of Natural Products
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Downregulation of KLF8 expression by shRNA induces inhibition of cell proliferation in CAL27 human oral cancer cells

2013

Objectives: KLF8 is a member of KLF transcription factors which play an important tolr in oncogenesis. It is barely expressed in normal human epithelial cells but highly overexpressed in several types of human cancer cell lines. In the present study, we investigate the role of KLF8 in oral cancer and the effects of KLF8 knockdown via lentivirus mediated siRNA infection in human adenosquamos carcinoma CAL 27 cells. Study Design: �e developed a vector-based siRNA expression system that can induce RNAi in CAL 27 oral canDesign: �e developed a vector-based siRNA expression system that can induce RNAi in CAL 27 oral canesign: �e developed a vector-based siRNA expression system that can induce RN…

Kruppel-Like Transcription FactorsDown-RegulationOdontologíaBiologymedicine.disease_causeSmall hairpin RNACarcinoma AdenosquamousDownregulation and upregulationmedicineTumor Cells CulturedGene silencingHumansRNA Small InterferingGeneral DentistryCell ProliferationGene knockdownOral Medicine and PathologyTransfection:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludRepressor Proteinsstomatognathic diseasesOtorhinolaryngologyCell cultureUNESCO::CIENCIAS MÉDICASCancer cellCancer researchLentivirus InfectionsSurgeryResearch-ArticleMouth NeoplasmsCarcinogenesisMedicina Oral, Patología Oral y Cirugía Bucal
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Inhibition of lactate export by quercetin acidifies rat glial cells in vitro

1997

The relationship between glial lactate release and glial intracellular pH (pH i) regulation is studied using C6 glioma cells and rat astrocytes in vitro, and the lactate transport inhibitors quercetin and a-cyano-4-hydroxycinnamate (CHC). pHi is measured using 2′,7′bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The results show that lactate release is mediated partly by a specific lactate transport system inhibitable by quercetin (50 mM), but not by CHC (5 mM). Inhibition by quercetin results in a significant 3‐4-fold increase of intracellular lactate and a decrease of intracellular pH to 6.9. A participation of quercetin-inhibitable lactate transport in glial pHi-regulation is suggested…

Lactate transportIntracellular pHBiologychemistry.chemical_compoundTumor Cells CulturedmedicineAnimalsheterocyclic compoundsLactic AcidFluorescent DyesGeneral NeuroscienceBiological TransportHydrogen-Ion ConcentrationFluoresceinsIn vitroRatsLactic acidmedicine.anatomical_structurechemistryBiochemistryCell cultureNeurogliaQuercetinQuercetinAcidsNeurogliaIntracellularNeuroscience Letters
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Increased expression of leptin and the leptin receptor as a marker of breast cancer progression: possible role of obesity-related stimuli.

2006

Abstract Purpose: Recent in vitro studies suggested that the autocrine leptin loop might contribute to breast cancer development by enhancing cell growth and survival. To evaluate whether the leptin system could become a target in breast cancer therapy, we examined the expression of leptin and its receptor (ObR) in primary and metastatic breast cancer and noncancer mammary epithelium. We also studied whether the expression of leptin/ObR in breast cancer can be induced by obesity-related stimuli, such as elevated levels of insulin, insulin-like growth factor-I (IGF-I), estradiol, or hypoxic conditions. Experimental Design: The expression of leptin and ObR was examined by immunohistochemistry…

LeptinCancer ResearchER-BETAmedicine.medical_treatmentHYPOXIA-INDUCIBLE FACTOR-1NeoplasmsTumor Cells CulturedBreastInsulin-Like Growth Factor Iskin and connective tissue diseasesReceptorAged 80 and overEstradiolIGF-I RECEPTORCELL-LINEReverse Transcriptase Polymerase Chain ReactionLeptindigestive oral and skin physiologyCarcinoma Ductal BreastMiddle AgedMetastatic breast cancerINSULINCell HypoxiaESTROGENOncologyDisease ProgressionIGF-I RECEPTOR; HYPOXIA-INDUCIBLE FACTOR-1; OB GENE; GROWTH-FACTOR; CELL-LINE; ER-BETA; ESTROGEN; ALPHA; INSULIN; MCF-7Receptors LeptinFemaleOB GENEhormones hormone substitutes and hormone antagonistsAdultmedicine.medical_specialtyGROWTH-FACTORBreast NeoplasmsReceptors Cell SurfaceBreast cancerInternal medicinemedicineBiomarkers TumorHumansObesityAutocrine signallingAgedLeptin receptorbusiness.industryInsulinmedicine.diseaseALPHAEndocrinologyTumor progressionCase-Control StudiesMCF-7business
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Functional analysis of the -2548G/A leptin gene polymorphism in breast cancer cells

2009

Leptin is overexpressed in human breast tumors and is produced by breast cancer cells in response to obesity-related stimuli. The leptin promoter polymorphism Lep-2548G/A can be associated with increased leptin secretion by adipocytes and elevated cancer risk. However, molecular mechanisms underlying the link between Lep-2548G/A and breast cancer have never been addressed. Lep-2548G/A is proximal to a binding site for the transcriptional factor Sp1. Furthermore nucleolin, a transcriptional repressor, can bind Sp1 or its consensus site. Consequently, we focused on the impact of Lep-2548G/A on Sp1- and nucleolin-dependent leptin transcription in breast cancer cells. The Lep-2548G/A was identi…

LeptinChromatin ImmunoprecipitationCancer Researchmedicine.medical_specialtyGenotypeSp1 Transcription FactorBlotting WesterneducationAdipokineBreast NeoplasmsBiologyBody Mass IndexBreast cancerInternal medicineTumor Cells CulturedmedicineHumansHypoglycemic AgentsInsulinObesityRNA MessengerPromoter Regions Genetichealth care economics and organizationsPolymorphism GeneticLeptin receptorReverse Transcriptase Polymerase Chain ReactionLeptinRNA-Binding ProteinsCancerPhosphoproteinsmedicine.diseaseEndocrinologyOncologyCancer researchImmunohistochemistryBreast diseaseNucleolinhormones hormone substitutes and hormone antagonistsInternational Journal of Cancer
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Insulin-dependent leptin expression in breast cancer cells.

2008

Abstract Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, and diabetes, seem to increase the risk of breast cancer. Here, we studied molecular mechanisms by which insulin activates the expression of leptin, an obesity hormone that has been shown to promote breast cancer progression in an autocrine or paracrine way. Using MDA-MB-231 breast cancer cells, we found that (a) insulin stimulated leptin mRNA and protein expression, which was associated with increased activation of the leptin gene promoter; (b) insulin increased nuclear accumulation of transcription factors hypoxia inducible factor (HIF)-1α and Sp1 and their loading on the leptin promoter;…

LeptinTranscriptional ActivationCancer Researchmedicine.medical_specialtySmall interfering RNAChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternFluorescent Antibody TechniqueBreast NeoplasmsEnzyme-Linked Immunosorbent AssayBiologyParacrine signallingPhosphatidylinositol 3-Kinasesbreast cancerInternal medicinemedicineHyperinsulinemiaTumor Cells CulturedHumansHypoglycemic AgentsInsulinRNA MessengerRNA Small InterferingAutocrine signallingLuciferasesPromoter Regions GeneticTranscription factorCell NucleusMitogen-Activated Protein Kinase 1Gene knockdownLeptin receptorMitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionLeptinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaEndocrinologyOncologyCancer researchFemalehormones hormone substitutes and hormone antagonistsCancer research
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[Apoptosis of human leukemic cells induced by topoisomerase I and II inhibitors].

1996

International audience; Comparison between five human leukemic lines (BV173, HL60, U937, K562, KCL22) suggest that the main determinant of their sensitivity to topoisomerase I (camptothecin) and II (VP-16) inhibitors is their ability to regulate cell cycle progression in response to specific DNA damage, then to die through apoptosis: the more the cells inhibit cell cycle progression, the less sensitive they are. The final pathway of apoptosis induction involves a cytoplasmic signal, active at neutral pH, needing magnesium, sensitive to various protease inhibitors and activated directly by staurosporine. Modulators of intracellular signaling (calcium chelators, calmodulin inhibitors, PKC mod…

Leukemia[SDV]Life Sciences [q-bio]Cell CycleApoptosisCell DifferentiationDNA Neoplasm[SDV.BC]Life Sciences [q-bio]/Cellular BiologyStaurosporine[SDV] Life Sciences [q-bio]AlkaloidsDNA Topoisomerases Type IIDNA Topoisomerases Type ITumor Cells CulturedHumansTopoisomerase II InhibitorsCamptothecinTopoisomerase I Inhibitors[SDV.BC] Life Sciences [q-bio]/Cellular BiologyProtein Kinase CEtoposideSignal Transduction
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