Search results for "antineoplastic agent"

showing 10 items of 1538 documents

Cytotoxicity of apigenin toward multiple myeloma cell lines and suppression of iNOS and COX-2 expression in STAT1-transfected HEK293 cells.

2020

Apigenin is one of the most abundant dietary flavonoids that possesses multiple bio-functions.This study was designed to determine the influence of apigenin on gene expressions, cancer cells, as well as STAT1/COX-2/iNOS pathway mediated inflammation and tumorigenesis in HEK293-STAT1 cells. Furthermore, the cytotoxic activity toward multiple myeloma (MM) cell lines was investigated.Bioinformatic analyses were used to predict the sensitivity and resistance of tumor cells toward apigenin and to determine cellular pathways influenced by this compound. The cytotoxic and ferroptotic activity of apigenin was examined by the resazurin reduction assay. Additionally, we evaluated apoptosis, and cell …

Programmed cell deathPharmaceutical ScienceNitric Oxide Synthase Type IIApoptosis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDrug DiscoveryAntineoplastic Combined Chemotherapy ProtocolsAutophagyCytotoxic T cellHumansDAPIApigenin030304 developmental biologyCell ProliferationPharmacology0303 health sciencesDose-Response Relationship DrugChemistryCell CycleComputational BiologyCell cycleAntineoplastic Agents PhytogenicHEK293 CellsSTAT1 Transcription FactorComplementary and alternative medicineApoptosisCell cultureCyclooxygenase 2Doxorubicin030220 oncology & carcinogenesisApigeninCancer cellCancer researchMolecular MedicineMultiple MyelomaReactive Oxygen SpeciesPhytomedicine : international journal of phytotherapy and phytopharmacology
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Pyrazolo[3,4-h]quinolines promising photosensitizing agents in the treatment of cancer.

2015

A new series of pyrazolo[3,4-h]quinolines, heteroanalogues of angelicin was conveniently prepared with a broad substitution pattern. A large number of derivatives was obtained and the cellular photocytotoxicity was evaluated in vitro against 5 different human tumor cell lines with GI50 values reaching the nanomolar level (14.52e0.04 mM). Selected compounds were able to photoinduce a massive cell death with the involvement of mitochondria. Their photodamage cellular targets were proteins and lipids and they did not cause any kind of DNA photodamage. This latter event is of considerable importance in the modulation of long term side effects, generally associated with the use of classical furo…

Programmed cell deathPhotodynamic therapy; Antiproliferative activity; Photosensitizing agents; Reactive oxygen species; PUVA therapyPUVA therapymedicine.medical_treatmentPhotodynamic therapyAntineoplastic AgentsAntiproliferative activityPhotodynamic therapy Antiproliferative activity Photosensitizing agents Reactive oxygen species PUVA therapyMitochondrionPhotodynamic therapychemistry.chemical_compoundStructure-Activity RelationshipAngelicinCell Line TumorDrug DiscoverymedicineStructure–activity relationshipHumansCell ProliferationPharmacologyPhotosensitizing AgentsDose-Response Relationship DrugMolecular StructureCell growthOrganic ChemistryGeneral MedicinePhotosensitizing AgentSettore CHIM/08 - Chimica FarmaceuticaFurocoumarinsBiochemistrychemistryQuinolinesPyrazolesDrug Screening Assays AntitumorReactive oxygen speciesEuropean journal of medicinal chemistry
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Apoptosis: a relevant tool for anticancer therapy.

2006

Apoptosis is a form of cell death that permits the removal of damaged, senescent or unwanted cells in multicellular organisms, without damage to the cellular microenvironment. Defective apoptosis represents a major causative factor in the development and progression of cancer. The majority of chemotherapeutic agents, as well as radiation, utilize the apoptotic pathway to induce cancer cell death. Resistance to standard chemotherapeutic strategies also seems to be due to alterations in the apoptotic pathway of cancer cells. Recent knowledge on apoptosis has provided the basis for novel targeted therapies that exploit apoptosis to treat cancer. These new target include those acting in the ext…

Programmed cell deathSettore MED/06 - Oncologia MedicaSurvivinAntineoplastic AgentsApoptosisLigandsInhibitor of Apoptosis ProteinsBortezomibTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSulindacExisulindNeoplasmsSurvivinmedicineAnimalsHumansbusiness.industryBortezomibapoptosis TRAIL/Apo2L apoptin/VP3 ONYX015 Bortezomib exisulind survivinCancerReceptors Death DomainHematologymedicine.diseaseBoronic AcidsNeoplasm ProteinsOncologyProteasomechemistryApoptosisPyrazinesCancer cellCancer researchCapsid ProteinsbusinessMicrotubule-Associated Proteinsmedicine.drug
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In Vitro and in Vivo Evaluation of Water-Soluble Iminophosphorane Ruthenium(II) Compounds. A Potential Chemotherapeutic Agent for Triple Negative Bre…

2014

A series of organometallic ruthenium(II) complexes containing iminophosphorane ligands have been synthesized and characterized. Cationic compounds with chloride as counterion are soluble in water (70–100 mg/mL). Most compounds (especially highly water-soluble 2) are more cytotoxic to a number of human cancer cell lines than cisplatin. Initial mechanistic studies indicate that the cell death type for these compounds is mainly through canonical or caspase-dependent apoptosis, nondependent on p53, and that the compounds do not interact with DNA or inhibit protease cathepsin B. In vivo experiments of 2 on MDA-MB-231 xenografts in NOD.CB17-Prkdc SCID/J mice showed an impressive tumor reduction (…

Programmed cell deathStereochemistryPhosphoranesAntineoplastic AgentsTriple Negative Breast NeoplasmsMice SCIDPharmacologyIn Vitro TechniquesArticleRutheniumIn vivoCoordination ComplexesMice Inbred NODDrug DiscoverymedicineOrganometallic CompoundsCytotoxic T cellAnimalsHumansCathepsinCisplatinChemistryWaterIn vitro3. Good healthHEK293 CellsSolubilityCell cultureApoptosisMolecular MedicineFemalemedicine.drugJournal of Medicinal Chemistry
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Combined inhibition of Bcl-2 and NFκB synergistically induces cell death in cutaneous T-cell lymphoma.

2019

Abstract Therapeutic options for cutaneous T-cell lymphoma (CTCL) are limited and curative treatment regimens are not available. Thus, new targeted and well-tolerated therapeutic approaches are urgently needed. In this respect, we have recently shown that dimethyl fumerate (DMF) inhibits NF-κB acting as a survival factor in CTCL. Similarly, inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) has been shown to induce cell death in CTCL especially when combined with histone deacetylase inhibitors. Therefore, we hypothesized that inhibition of Bcl-2 should potentiate NF-κB inhibition in a novel combination treatment of CTCL. We show that, in vitro, the Bcl-2 inhibitors ABT-199 an…

Programmed cell deathT cellImmunologyAntineoplastic AgentsApoptosisBiochemistryMicehemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansRNA Small InterferingCell ProliferationNeoplasm StagingCell DeathDose-Response Relationship Drugbusiness.industryCutaneous T-cell lymphomaNF-kappa BDrug SynergismCell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysLymphomaLymphoma T-Cell CutaneousHistone Deacetylase InhibitorsDisease Models Animalmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCancer researchRNA InterferenceHistone deacetylaseSignal transductionbusinessProtein BindingBlood
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Autophagy-Dependent Anticancer Immune Responses Induced by Chemotherapeutic Agents in Mice

2011

Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity. In response to chemotherapy, autophagy-competent, but not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited the release of adenosine triphosphate (ATP) from dying tumor cells. Conversely, inhibition of extracellular ATP-degrading enzymes increased pericellular ATP in autophagy-deficient tumors, reestablished the recr…

Programmed cell deathcells cancer immunogenicity calreticulin exposure hmgb1Antineoplastic AgentsBiologyimmunogenicityNOMicechemistry.chemical_compoundAdenosine TriphosphateImmune systemCell Line TumorNeoplasmsAutophagyExtracellularAnimalsHumanscancerMice Inbred BALB CMultidisciplinaryCell DeathImmunogenicityAutophagyDendritic CellsMice Inbred C57BLhmgb1chemistryCell cultureCancer researchImmunogenic cell deathcellsMitoxantroneCalreticulinAdenosine triphosphatecalreticulin exposure
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Programmed cell death (PCD) associated with the stilbene motif of arotinoids: discovery of novel apoptosis inducer agents possessing activity on mult…

2000

Considering that the stereochemistry of the C9-C10 alkenyl portion of natural 9-cis-RA, as the one of the olefinic moiety of the previously described isoxazole retinoid 4, seems of particular importance for their apoptotic activity, we prepared a novel class of TTNPB analogues bearing both the cis or trans configuration of the alkenyl portion. The compounds were evaluated in vitro for their cytotoxic and apoptotic activities. We discovered that the cis-TTNPB 9c possesses apoptotic activity comparable with that of the retinoid 4. Moreover, the amino arotinoid 16c showed potent apoptotic activity in HL60 promyelocytic leukemia cells. Interestingly, 16c proved to be a particularly potent apopt…

Programmed cell deathmedicine.drug_classHL60Clinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsApoptosisHL-60 CellsBiochemistryRetinoidschemistry.chemical_compoundStilbenesDrug DiscoverymedicineHumansCytotoxic T cellRetinoidCytotoxicityMolecular BiologyChemistryOrganic ChemistryDrug Resistance MultipleMultiple drug resistanceBiochemistryApoptosisCell cultureMolecular MedicineK562 CellsBioorganic & Medicinal Chemistry Letters
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Berberine inhibits cell growth and mediates caspase-independent cell death in human pancreatic cancer cells.

2010

Pancreatic cancer is one of the most aggressive human malignancies with an increasing incidence worldwide. In addition to the poor survival rates, combinations using gemcitabine as a backbone have failed to show any benefit beyond monotherapy. These facts underscore an urgent need for novel therapeutic options and motivated us to study the effect of berberine on pancreatic cancer cells. Here, we undertook an mRNA-based gene expression profiling study in order to get deeper insight into the molecular targets mediating the growth inhibitory effects of berberine on pancreatic cancer cells compared to normal ones. Twenty-four hours after treatment, berberine showed preferential selectivity towa…

Programmed cell deathmedicine.medical_specialtyBerberineDNA damagePharmaceutical ScienceApoptosisAnalytical Chemistrychemistry.chemical_compoundBerberinePancreatic cancerInternal medicineCell Line TumorDrug DiscoverymedicineHumansRNA MessengerCell ProliferationOligonucleotide Array Sequence AnalysisPharmacologybiologyCell growthTopoisomeraseGene Expression ProfilingOrganic ChemistryCancermedicine.diseaseAntineoplastic Agents PhytogenicCaspase InhibitorsImmunohistochemistryEnzyme ActivationPancreatic NeoplasmsEndocrinologyComplementary and alternative medicinechemistryApoptosisCaspasesbiology.proteinCancer researchMolecular MedicineSignal TransductionPlanta medica
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NF-κB Inhibition Restores Sensitivity to Fas-Mediated Apoptosis in Lymphoma Cell Lines

2003

Failure to perform the Fas-related apoptosis pathway can account for tumor resistance both to chemotherapeutic agents and to immunological effectors. We studied the role of NK-kappaB in Fas-resistance, employing the Fas-sensitive human T-lymphoma HuT78 cell line and its Fas-resistant variants HuT78B1 and HuT78G9. All these cell lines expressed high levels of constitutively activated NF-kappaB. Pretreatment of cells with NF-kappaB inhibitors (PDTC, MG132, or SN50) strongly enhanced CH11-induced apoptosis in HuT78 and Hut78G9 cells, while only MG132 showed a similar potentiating effect in HuT78B1. The described synergism was significantly inhibited by pretreatment with the anti-Fas-blocking a…

ProlineLeupeptinsT cellAntineoplastic AgentsApoptosisBiologyLymphoma T-CellGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundHistory and Philosophy of ScienceThiocarbamatesCell Line TumorMG132medicineHumansfas Receptorapoptosis NF-KappaB MG132 Fas/FasL systemEffectorGeneral NeuroscienceNF-kappa BNF-κBmedicine.diseaseMolecular biologyLymphomamedicine.anatomical_structurechemistryApoptosisCell culturebiology.proteinAntibodyPeptidesAnnals of the New York Academy of Sciences
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Multi-output Model with Box-Jenkins Operators of Quadratic Indices for Prediction of Malaria and Cancer Inhibitors Targeting Ubiquitin- Proteasome Pa…

2016

The ubiquitin-proteasome pathway (UPP) is the primary degradation system of short-lived regulatory proteins. Cellular processes such as the cell cycle, signal transduction, gene expression, DNA repair and apoptosis are regulated by this UPP and dysfunctions in this system have important implications in the development of cancer, neurodegenerative, cardiac and other human pathologies. UPP seems also to be very important in the function of eukaryote cells of the human parasites like Plasmodium falciparum, the causal agent of the neglected disease Malaria. Hence, the UPP could be considered as an attractive target for the development of compounds with Anti-Malarial or Anti-cancer properties. R…

Proteasome Endopeptidase ComplexDNA repairDatabases PharmaceuticalAntineoplastic AgentsComputational biologyBioinformatics01 natural sciencesBiochemistryAntimalarialsUbiquitinNeoplasmsDrug DiscoveryHumansMolecular Targeted TherapyMolecular BiologybiologyDrug discoveryUbiquitinComputational BiologyCell BiologyGeneral MedicineCell cyclechEMBL0104 chemical sciencesMalaria010404 medicinal & biomolecular chemistryProteasomeProteolysisbiology.proteinSignal transductionFunction (biology)Current proteinpeptide science
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