Search results for "Viability assay"

showing 10 items of 279 documents

In vitro evaluation of biomimetic chitosan-calcium phosphate scaffolds with potential application in bone tissue engineering.

2013

This work reports on the physicochemical properties and in vitro cytotoxicity assessment of chitosan–calcium phosphate (Cs–CP) scaffolds for bone tissue engineering, which were synthesized by a novel biomimetic co-precipitation method. X-ray diffraction (XRD) along with scanning electron microscopy (SEM) analysis confirmed the porous morphology of the scaffolds and the amorphous nature of the inorganic phase with different crystallite sizes and the formation of various forms of calcium phosphate. Compressive mechanical testing revealed that the Young’s modulus of the biomaterials is in the range of human trabecular bone. In vitro tests were performed on the biomaterials for up to 14 days to…

Calcium PhosphatesMaterials scienceCompressive StrengthCell SurvivalBiomedical EngineeringBioengineeringBone remodelingCell LineBiomaterialschemistry.chemical_compoundIn vivoBiomimetic MaterialsHardnessElastic ModulusMaterials TestingmedicineHumansViability assayCytotoxicityChitosanOsteoblastsOsteoblastIn vitroVascular endothelial growth factormedicine.anatomical_structurechemistryCell cultureBone SubstitutesBiophysicsBiomedical engineeringBiomedical materials (Bristol, England)
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Activity of the dietary flavonoid, apigenin, against multidrug-resistant tumor cells as determined by pharmacogenomics and molecular docking

2015

Apigenin is a common dietary flavonoid with considerable cytotoxic activity in vitro and in vivo. Despite many mechanistic studies, less is known about resistance factors hampering apigenin's activity. We investigated the ATP-binding cassette (ABC) transporters BCRP/ABCG2, P-glycoprotein/ABCB1 and its close relative ABCB5. Multidrug-resistant cells overexpressing these ABC transporters were not cross-resistant toward apigenin. Moreover, apigenin inhibited not only P-glycoprotein but also BCRP by increasing cellular uptake of doxorubicin and synergistic inhibition of cell viability in combination with doxorubicin or docetaxel in multidrug-resistant cells. To perform in silico molecular docki…

Cancer ResearchAbcg2Protein ConformationEndocrinology Diabetes and MetabolismClinical BiochemistryATP-binding cassette transporterPharmacologyBiochemistryMicechemistry.chemical_compoundTranscriptional regulationCluster AnalysisImmunology and AllergyApigeninNutrition and DieteticsbiologyABCB5Drug Resistance MultipleNeoplasm ProteinsMolecular Docking SimulationOncologyBiochemistryApigeninMolecular Medicinemedicine.drugIn silicoImmunologyInhibitory Concentration 50Cell Line TumormedicineAnimalsHumansDoxorubicinATP Binding Cassette Transporter Subfamily B Member 1RNA MessengerViability assayMolecular BiologyPharmacologyComputational BiologyPolyphenolsTransporterIn vitroHEK293 CellschemistryDoxorubicinDrug Resistance NeoplasmPharmacogeneticsPoster Presentationbiology.proteinATP-Binding Cassette TransportersThe Journal of Nutritional Biochemistry
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In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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The potential of acetaminophen as a prodrug in gene-directed enzyme prodrug therapy.

2000

Acetaminophen is oxidized by human CYP1A2 to the cytotoxic metabolite N-acetylbenzoquinoneimine (NABQI). Incubation of cells transfected with human CYP1A2 (H1A2 MZ cells) with 4-20 mM acetaminophen for 6 hours at 37 degrees C caused extensive cytotoxicity (cell viability10%). In contrast, nontransfected V79 MZ cells were unaffected (viability95%). By mixing H1A2 MZ cells with V79 MZ cells in various proportions and incubating with 4 mM acetaminophen, it was shown that the NABQI released from H1A2 MZ cells also caused cytotoxicity of bystander cells. Thus, in a mixture containing 5% H1A2 MZ cells, exposure to 4 mM acetaminophen for 6 hours resulted in complete cell killing by 24 hours. A sim…

Cancer ResearchCell SurvivalPharmacologyTransfectionCatalysisCell LineCricetulusCytochrome P-450 CYP1A2CricetinaemedicineTumor Cells CulturedCytotoxic T cellAnimalsHumansProdrugsViability assayCytotoxicityMolecular BiologyAcetaminophenChemistryCYP1A2TransfectionGenetic TherapyProdrugAcetaminophenCell killingMolecular Medicinemedicine.drugCancer gene therapy
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The Impact of Insulin on Low-dose Metronomic Vinorelbine and Mafosfamide in Breast Cancer Cells

2021

Background/aim Breast cancer (BC) may be affected by diabetes and anti-diabetic medication, as well as its therapeutic agents. Low-dose metronomic chemotherapy (LDMC) is an available treatment option in BC. We investigated the impact of insulin on low-dose metronomic vinorelbine and mafosfamide in BC cell lines. Materials and methods Human BC cell lines T-47D, MCF-7, MDA-MB-231, BT-549 and non-tumorigenic breast cell line MCF-10A were exposed to 0.01 μg/ml and 10 μg/ml insulin in combination with low-dose metronomic vinorelbine or mafosfamide. The cell viability was determined after 24-72 hours using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Results Insulin, especi…

Cancer ResearchCell Survivalmedicine.medical_treatmentAntineoplastic AgentsBreast NeoplasmsPharmacologyVinorelbinechemistry.chemical_compoundBreast cancerMafosfamideCell Line TumormedicineHumansInsulinCytotoxic T cellViability assayCyclophosphamidebusiness.industryInsulinVinorelbineGeneral Medicinemedicine.diseaseMetronomic ChemotherapyOncologychemistryAdministration MetronomicFemalebusinessmedicine.drugHormoneAnticancer Research
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Abstract 1138: The protein disulfide isomerase inhibitor XCE853 inhibits in vitro, ex-vivo and in vivo growth of human tumors

2017

Abstract Protein disulfide isomerase (PDI) is a chaperone protein that regulates oxidative protein folding as well as cell viability. Increased PDI levels have been documented in a variety of human cancers associated with a poor overall survival, including ovarian, prostate, brain and lung cancers. Inhibition of PDI activity leads to apoptosis in cancer, suggesting that PDI is a promising druggable target. XCE853 is a synthetic small molecule displaying an excellent docking with the catalytic domain of the human PDI. XCE853 inhibits in vitro recombinant PDI enzymatic activity. In addition, the proliferation of a large panel of human tumor cells is blocked by XCE853 with IC50s in the nanomol…

Cancer ResearchChemistryCancerProtein aggregationmedicine.diseaseMolecular biologyIn vitroCytolysisOncologyApoptosisIn vivomedicineViability assayProtein disulfide-isomeraseCancer Research
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Selectivity analysis of protein kinase CK2 inhibitors DMAT, TBB and resorufin in cisplatin-induced stress responses.

2009

Udgivelsesdato: 2009-Nov Targeting protein kinases as a therapeutic approach to treat various diseases, especially cancer is currently a fast growing business. Although many inhibitors are available, exhibiting remarkable potency, the major challenge is their selectivity. Here we show that the protein kinase CK2 inhibitors DMAT, TBB and resorufin differ in their selectivity against PI3K family members, since PI3K and DNA-PK are subject to inhibition by DMAT and TBB, however, not by resorufin. TBB and DMAT treatment together with cisplatin lead to an inhibition of cisplatin-induced stress signaling (as detected by phosphorylation of JNK and H2AX). In the case of resorufin no interference wit…

Cancer ResearchKinaseCell SurvivalBlotting WesternAntineoplastic AgentsCell cycleBiologyTriazolesCell killingOncologyBiochemistryApoptosisStress PhysiologicalCell Line TumorOxazinesPhosphorylationHumansBenzimidazolesViability assayCasein kinase 2Signal transductionCisplatinEnzyme InhibitorsCasein Kinase IISignal TransductionInternational journal of oncology
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WIN induces apoptotic cell death in human colon cancer cells through a block of autophagic flux dependent on PPARγ down-regulation.

2014

Cannabinoids have been reported to possess anti-tumorigenic activity in cancer models although their mechanism of action is not well understood. Here, we show that the synthetic cannabinoid WIN55,212-2 (WIN)-induced apoptosis in colon cancer cell lines is accompanied by endoplasmic reticulum stress induction. The formation of acidic vacuoles and the increase in LC3-II protein indicated the involvement of autophagic process which seemed to play a pro-survival role against the cytotoxic effects of the drug. However, the enhanced lysosomal membrane permeabilization (LMP) blocked the autophagic flux after the formation of autophagosomes as demonstrated by the accumulation of p62 and LC3, two ma…

Cancer ResearchMorpholinesClinical BiochemistryPharmaceutical ScienceDown-RegulationAntineoplastic AgentsApoptosisBiologyNaphthalenesDownregulation and upregulationSettore BIO/10 - BiochimicaCell Line TumormedicineAutophagyGene silencingHumansViability assayPharmacologyEndoplasmic reticulumBiochemistry (medical)AutophagyCannabinoids PPARγ ER stress autophagy/apoptosis interplay colon carcinoma cellsCell BiologyEndoplasmic Reticulum StressCell biologyBenzoxazinesMitochondriaPPAR gammaMechanism of actionApoptosisColonic NeoplasmsUnfolded protein responsemedicine.symptomSignal TransductionApoptosis : an international journal on programmed cell death
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Relation of early Photofrin uptake to photodynamically induced phototoxicity and changes of cell volume in different cell lines.

1994

For efficacy of photodynamic therapy, selective uptake and retention of photoactive substances has been postulated. Therefore, measurements were performed to find out whether the photosensitiser Photofrin® is taken up differently in malignant and non-malignant cells in vitro . In addition, the sensitivity of malignant cells and nonmalignant cells to photodynamic exposure was investigated, by quantifying viability and volume alterations of the cells. Bovine aortic endothelial cells, mouse fibroblasts and amelanotic hamster melanoma cells were suspended in a specially designed incubation chamber under controlled conditions (e.g. pH, p O 2 , p CO 2 and temperature). After establishing constant…

Cancer ResearchPathologymedicine.medical_specialtyCell Survivalmedicine.medical_treatmentCellPhotodynamic therapyBiologyFlow cytometryMiceCricetinaemedicineTumor Cells CulturedAnimalsPhotosensitizerViability assayFibroblastMelanomaCells Culturedmedicine.diagnostic_testMesocricetusFibroblastsmedicine.anatomical_structureOncologyPhotochemotherapyCell cultureCancer researchCattleDihematoporphyrin EtherEndothelium VascularPhototoxicityEuropean journal of cancer (Oxford, England : 1990)
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Sodium phenylbutyrate induces apoptosis in human retinoblastoma Y79 cells: The effect of combined treatment with the topoisomerase I-inhibitor topote…

2001

Our results demonstrate that sodium phenylbutyrate, a compound with a low degree of toxicity, exerted a cytotoxic effect on human retinoblastoma Y79 cells in a time- and dose-dependent manner. Treatment of Y79 cells for 72 h with phenylbutyrate reduced cell viability by 63% at 2 mM and 90% at 4 mM. Cell death caused by phenylbutyrate exhibited the typical features of apoptosis, as shown by light and fluorescent microscopy. Western blot analysis demonstrated that exposure of Y79 cells to phenylbutyrate decreased the level of the antiapoptotic factor Bcl-2 and induced the activation of caspase-3, a key enzyme in the execution phase of apoptosis. Moreover, treatment with phenylbutyrate markedl…

Cancer ResearchProgrammed cell deathCell SurvivalBlotting WesternApoptosisPhenylbutyrateHistonesSettore BIO/10 - BiochimicamedicineTumor Cells CulturedHumansretinoblastoma apoptosis sodium phenylbutirateViability assayEnzyme InhibitorsbiologyCaspase 3TopoisomeraseRetinoblastomaSodium phenylbutyrateAcetylationDrug SynergismCell cyclePhenylbutyrateseye diseasesEnzyme ActivationOncologyProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinCancer researchTopotecanDrug Therapy CombinationTopoisomerase I InhibitorsTumor Suppressor Protein p53Topotecanmedicine.drug
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