Search results for "tumor cell"

showing 10 items of 694 documents

Parathyroid hormone-related peptide and 8701-BC breast cancer cell growth and invasion in vitro: evidence for growth-inhibiting and invasion-promotin…

1995

It has been previously reported that 8701-BC cells, derived from a primary carcinoma of the breast, constitutively express parathyroid hormone-related peptide (PTHrP) gene and that N-terminal PTHrP immunoreactivity can be found in cell medium. Here we have firstly measured immunoreactive PTHrP in 8701-BC cell medium using antibodies raised against midregion and C-terminal fragments, and also demonstrated the expression of PTH/PTHrP receptor by 8701-BC cells. Secondly, we have examined the role, if any, elicited by diverse PTHrP domains on 8701-BC cell proliferation, and invasive behaviour in vitro related to production of extracellular proteolytic enzymes. Our data show that PTHrP [1-34], a…

musculoskeletal diseasesmedicine.medical_specialtyCell divisionMolecular Sequence DataParathyroid hormoneBreast NeoplasmsBiologyPolymerase Chain ReactionBiochemistryEndocrinologyInternal medicineEndopeptidasesTumor Cells CulturedmedicineExtracellularHumansNeoplasm InvasivenessProtease InhibitorsRNA MessengerReceptorMolecular BiologyReceptor Parathyroid Hormone Type 1Base SequenceParathyroid hormone-related proteinCell growthParathyroid Hormone-Related ProteinProteolytic enzymesProteinsRNA-Directed DNA PolymeraseIn vitroEndocrinologyParathyroid HormoneCancer researchReceptors Parathyroid HormoneCell Divisionhormones hormone substitutes and hormone antagonistsMolecular and Cellular Endocrinology
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Extracellular matrix regulation of PTHrP and PTH/PTHrP receptor in a human breast cancer cell line

1999

AbstractIt was previously reported that 8701-BC breast cancer cells express the gene for parathyroid hormone-related peptide (PTHrP) and its cognate receptor (PTHrP-R), and release immunoreactive PTHrP in the extracellular medium; it was also found that PTHrP, in turn, exerts a role on the proliferative and invasive behavior in vitro of the same cell line. On the other hand, evidence has been produced that adhesion of 8701-BC cells onto different collagen substrates influences in various ways a number of phenotypic expressions, such as cell growth, motility, invasion of reconstituted basement membrane and production of lytic enzymes of the extracellular matrix (ECM). In light of these previ…

musculoskeletal diseasesmedicine.medical_specialtyParathyroid hormone-related peptideStromal cellRNA SplicingCellular differentiationBiophysicsBreast NeoplasmsBiologyPolymerase Chain ReactionBiochemistryExtracellular matrixBreast cancerStructural BiologyLamininInternal medicineGene expressionTumor Cells CulturedGeneticsmedicineExtracellularHumansParathyroid hormone-related peptide receptorMolecular BiologyReceptor Parathyroid Hormone Type 1Basement membraneParathyroid Hormone-Related ProteinProteinsCell DifferentiationCell Biologymusculoskeletal systemExtracellular MatrixNeoplasm ProteinsCell biologyGene Expression Regulation NeoplasticDrug CombinationsEndocrinologymedicine.anatomical_structureCell culturebiology.proteinReceptors Parathyroid HormoneProteoglycansGene expressionCollagenLamininhormones hormone substitutes and hormone antagonistsFEBS Letters
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Potential use of organotin(IV)-tripetide complexes as stopper in tumor cells growth.

2008

organotin(IV) tripeptide tumor cellsSettore CHIM/03 - Chimica Generale E Inorganica
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Intron variants of the p53 gene are associated with increased risk for ovarian cancer but not in carriers of BRCA1 or BRCA2 germline mutations

1999

Two biallelic polymorphisms in introns 3 and 6 of the p53 gene were analysed for a possible risk-modifying effect for ovarian cancer. Germline DNA was genotyped from 310 German Caucasian ovarian cancer patients and 364 healthy controls. We also typed 124 affected and 276 unaffected female carriers with known deleterious BRCA1 or BRCA2 germline mutation from high-risk breast-ovarian cancer families. Genotyping was based on PCR and high-resolution gel electrophoresis. German ovarian cancer patients who carried the rare allele of the MspI restriction fragment length polymorphism (RELP) in intron 6 were found to have an overall 1.93-fold increased risk (95% confidence internal (CI) 1.27–2.91) w…

p53AdultCancer Researchendocrine system diseasesAdolescentGenotypeGenes BRCA1BiologypolymorphismGermline mutationRisk FactorsGenotypemedicineTumor Cells CulturedHumansAlleleAllele frequencyGerm-Line MutationAgedGeneticsAged 80 and overBRCA2 ProteinOvarian NeoplasmsGenetic Carrier ScreeningCancerGenetic VariationRegular ArticleMiddle Agedmedicine.diseaseBRCA2 ProteinBRCA1Genes p53BRCA2IntronsNeoplasm Proteinsovarian cancerOncologyCase-Control StudiesCancer researchFemaleRestriction fragment length polymorphismOvarian cancergenetic susceptibilityTranscription FactorsBritish Journal of Cancer
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Apollon gene silencing induces apoptosis in breast cancer cells via p53 stabilisation and caspase-3 activation

2009

We analysed the effects of small interfering RNA (siRNA)-mediated silencing of Apollon, a member of the inhibitors of apoptosis protein family, on the proliferative potential and ability of human breast cancer cell lines to undergo apoptosis. In wild-type p53 ZR75.1 cells, Apollon knockdown resulted in a marked, time-dependent decline of cell growth and an increased rate of apoptosis, which was associated with p53 stabilisation and activation of the mitochondrial-dependent apoptotic pathway. Pre-incubation of cells with a p53-specific siRNA resulted in a partial rescue of cell growth inhibition, as well as in a marked reduction of the apoptotic response, indicating p53 as a major player in …

p53Cancer ResearchSmall interfering RNAProgrammed cell deathcaspase-3ApollonCaspase 3Breast NeoplasmsApollon gene apoptosisBiologyModels BiologicalInhibitor of Apoptosis ProteinsRNA interferenceTumor Cells CulturedGene silencingHumansGene SilencingRNA Small InterferingCell Proliferationhuman breast cancerGene knockdownCell growthCaspase 3Protein StabilityapoptosisEnzyme ActivationOncologyApoptosissiRNACancer researchSettore BIO/14 - FarmacologiaFemaleTumor Suppressor Protein p53Translational Therapeutics
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Anti tumor action of the natural compound parthenolide

2010

parthenolideSettore BIO/10 - Biochimicatumor cellsapoptosi
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Rac1-Regulated Endothelial Radiation Response Stimulates Extravasation and Metastasis That Can Be Blocked by HMG-CoA Reductase Inhibitors

2011

Radiotherapy (RT) plays a key role in cancer treatment. Although the benefit of ionizing radiation (IR) is well established, some findings raise the possibility that irradiation of the primary tumor not only triggers a killing response but also increases the metastatic potential of surviving tumor cells. Here we addressed the question of whether irradiation of normal cells outside of the primary tumor augments metastasis by stimulating the extravasation of circulating tumor cells. We show that IR exposure of human endothelial cells (EC), tumor cells (TC) or both increases TC-EC adhesion in vitro. IR-stimulated TC-EC adhesion was blocked by the HMG-CoA reductase inhibitor lovastatin. Glycyrr…

rac1 GTP-Binding ProteinPathologyCancer TreatmentToxicologyPolymerase Chain ReactionMetastasisMetastasisMiceCirculating tumor cellMolecular Cell BiologyBasic Cancer ResearchNeoplasm MetastasisMice Inbred BALB CMultidisciplinarybiologyChemistryQRTotal body irradiationPrimary tumorExtravasationOncologyMedicineElectrophoresis Polyacrylamide GelLovastatinE-SelectinWhole-Body IrradiationResearch Articlemedicine.drugDrugs and Devicesmedicine.medical_specialtyGenetic ToxicologyScienceBlotting WesternRadiation TherapyCardiovascular PharmacologyE-selectinCell AdhesionmedicineAnimalsHumansLovastatinCell adhesionBiologyDNA PrimersBase SequenceGlycyrrhizic Acidmedicine.diseaseCancer researchbiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsExtravasation of Diagnostic and Therapeutic MaterialsPLoS ONE
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Delivery of proteins into living cells by reversible membrane permeabilization with streptolysin-O

2001

The pore-forming toxin streptolysin O (SLO) can be used to reversibly permeabilize adherent and nonadherent cells, allowing delivery of molecules with up to 100 kDa mass to the cytosol. Using FITC-labeled albumin, 10 5 –10 6 molecules were estimated to be entrapped per cell. Repair of toxin lesions depended on Ca 2+ -calmodulin and on intact microtubules, but was not sensitive to actin disruption or to inhibition of protein synthesis. Resealed cells were viable for days and retained the capacity to endocytose and to proliferate. The active domains of large clostridial toxins were introduced into three different cell lines. The domains were derived from Clostridium difficile B-toxin and Clo…

rho GTP-Binding ProteinsCell Membrane PermeabilityGlycosylationCell SurvivalBacterial ToxinsClostridium difficile toxin AClostridium difficile toxin BBiologymedicine.disease_causeCell LineBacterial ProteinsAlbuminsChlorocebus aethiopsTumor Cells CulturedmedicineAnimalsHumansSecretionParticle SizeActinMultidisciplinaryDose-Response Relationship DrugSecretory VesiclesProteinsBiological TransportDextransBiological SciencesActin cytoskeletonMolecular biologyRatsCell biologyCytosolImmunoglobulin GCOS CellsStreptolysinsras ProteinsClostridium botulinumStreptolysinProceedings of the National Academy of Sciences
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Inhibition of small G proteins of the Rho family by statins orClostridium difficiletoxin B enhances cytokine-mediated induction of NO synthase II

2000

In order to investigate the involvement of Ras and/or Rho proteins in the induction of the inducible isoform of nitric oxide synthase (NOS II) we used HMG-CoA reductase inhibitors (statins) and Clostridium difficile toxin B (TcdB) as pharmacological tools. Statins indirectly inhibit small G proteins by preventing their essential farnesylation (Ras) and/or geranylgeranylation (Rho). In contrast, TcdB is a glucosyltransferase and inactivates Rho-proteins directly. Human A549/8- and DLD-1 cells as well as murine 3T3 fibroblasts were preincubated for 18 h with statins (1–100 μM) or TcdB (0.01–10 ng ml−1). Then NOS II expression was induced by cytokines. NOS II mRNA was measured after 4–8 h by R…

rho GTP-Binding ProteinsG proteinBacterial ToxinsMevalonic AcidNitric Oxide Synthase Type IISmall G ProteinClostridium difficile toxin BBiologyGene Expression Regulation EnzymologicMiceGeranylgeranylationBacterial ProteinsPolyisoprenyl PhosphatesPrenylationGTP-Binding ProteinsGene expressionAtorvastatinTumor Cells CulturedAnimalsHumansDrug InteractionsPyrrolesLovastatinPromoter Regions GeneticPharmacology3T3 CellsTransfectionMolecular biologyHeptanoic AcidsEnzyme InductionPapersCytokinesHydroxymethylglutaryl-CoA Reductase InhibitorsNitric Oxide SynthaseSignal transductionBritish Journal of Pharmacology
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Effects of ectopic expression of NGAL on doxorubicin sensitivity.

2012

Neutrophil gelatinase-associated lipocalin (NGAL, a.k.a Lnc2) is a member of the lipocalin family which has diverse roles including stabilizing matrix metalloproteinase-9 from auto-degradation and as siderocalins which are important in the transport of iron. NGAL also has important biological functions involved in immunity and inflammation as well as responses to kidney damage. NGAL expression has also been associated with certain neoplasia and is important in the metastasis of breast cancer. Many advanced cancer patients have elevated levels of NGAL in their urine and it has been proposed that NGAL may be a prognostic indicator for certain cancers (e.g. breast, brain, and others). NGAL exp…

siderocalinColorectal cancerBlotting WesternResistanceBreast NeoplasmsLipocainBiologyLipocalinsiderocalinsMetastasisBreast cancerLcn2Lipocalin-2Proto-Oncogene ProteinsmedicineTumor Cells CulturedHumansDoxorubicinNGALIron transportCell Proliferationdrug resistanceAntibiotics AntineoplasticCancermedicine.diseaseResearch PapersLipocalinsOncologyDocetaxelDrug Resistance NeoplasmDoxorubicinImmunologyCancer researchDoxorubicin; Drug resistance; Iron transport; Lcn2; Lipocalins; MMP-9; NGAL; SiderocalinsEctopic expressionFemalelipocalinMMP-9Colorectal Neoplasmsmedicine.drugAcute-Phase Proteins
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