Search results for "cancer cell"

showing 10 items of 756 documents

Hsp60 is actively secreted by human tumor cells

2010

Background Hsp60, a Group I mitochondrial chaperonin, is classically considered an intracellular chaperone with residence in the mitochondria; nonetheless, in the last few years it has been found extracellularly as well as in the cell membrane. Important questions remain pertaining to extracellular Hsp60 such as how generalized is its occurrence outside cells, what are its extracellular functions and the translocation mechanisms that transport the chaperone outside of the cell. These questions are particularly relevant for cancer biology since it is believed that extracellular chaperones, like Hsp70, may play an active role in tumor growth and dissemination. Methodology/Principal Findings S…

Cell SurvivalBlotting WesternCellImmunology/Immunomodulationlcsh:MedicineApoptosisBiologyExosomesCell LineAmilorideCell membraneMicroscopy Electron TransmissionCell Line TumorNeoplasmsBiochemistry/Cell Signaling and Trafficking StructuresExtracellularmedicineHumansSecretionlcsh:ScienceMultidisciplinarySettore BIO/16 - Anatomia Umanabeta-Cyclodextrinslcsh:RChaperonin 60MicrovesiclesCell biologyPathology/PathophysiologyHSP60 Mitochondria Chaperonopatiesmedicine.anatomical_structureCell cultureCulture Media ConditionedCancer cellAcetylcholinesteraselcsh:QExtracellular SpaceK562 CellsIntracellularResearch Article
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Cytotoxicity of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide in multidrug-resistant cancer cells through activation of PERK/eIF2α/AT…

2021

After decades of research, multidrug resistance (MDR) remains a huge challenge in cancer treatment. In this study, the cytotoxic of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide (MCC1734) has been investigated towards multidrug-resistant cancer cell lines. MCC1734 exerted cytotoxicity on cell lines expressing different mechanisms of drug resistance (P-glycoprotein, BCRP, ABCB5, EGFR, p53 knockout) to a different extent. Interestingly, sensitive CCRF-CEM cells and multidrug-resistant P-gp-overexpressing CEM/ADR5000 cells represented similar sensitivity towards MCC1734, indicating MCC1734 can bypass P-gp-mediated resistance. Microarray-based mRNA expression revealed that MCC17…

Cell SurvivalEukaryotic Initiation Factor-2Antineoplastic AgentsMitochondrionBiochemistryFlow cytometryeIF-2 KinaseCell Line TumorOxazinesmedicineHumansCytotoxic T cellGene Regulatory NetworksCytotoxicityPharmacologyMolecular Structuremedicine.diagnostic_testChemistryCell cycleActivating Transcription Factor 4Gene Expression Regulation NeoplasticXanthenesDrug Resistance NeoplasmCell cultureApoptosisCancer cellCancer researchGene DeletionBiochemical Pharmacology
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Inhibition of stearoyl-CoA desaturase 1 expression induces CHOP-dependent cell death in human cancer cells.

2010

Background Cancer cells present a sustained de novo fatty acid synthesis with an increase of saturated and monounsaturated fatty acid (MUFA) production. This change in fatty acid metabolism is associated with overexpression of stearoyl-CoA desaturase 1 (Scd1), which catalyses the transformation of saturated fatty acids into monounsaturated fatty acids (e.g., oleic acid). Several reports demonstrated that inhibition of Scd1 led to the blocking of proliferation and induction of apoptosis in cancer cells. Nevertheless, mechanisms of cell death activation remain to be better understood. Principal Findings In this study, we demonstrated that Scd1 extinction by siRNA triggered abolition of de nov…

Cell SurvivalEukaryotic Initiation Factor-2lcsh:MedicineApoptosisCHOPBiologyCell Biology/Cell SignalingCell Linechemistry.chemical_compoundCell Line TumorNeoplasmsHumansRNA Small Interferinglcsh:ScienceEndoplasmic Reticulum Chaperone BiPFatty acid synthesisHeat-Shock ProteinsCell ProliferationTranscription Factor CHOPMultidisciplinaryFatty acid metabolismCell DeathCell growthFatty Acidslcsh:RCell Biology/Cellular Death and Stress ResponsesMolecular biologyCell biologychemistryOncologyApoptosisCancer celllipids (amino acids peptides and proteins)lcsh:QStearoyl-CoA desaturase-1Stearoyl-CoA DesaturaseTranscription Factor CHOPResearch ArticleOleic AcidPLoS ONE
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Identification of new P-glycoprotein inhibitors derived from cardiotonic steroids

2014

P-glycoprotein (ABCB1, MDR1) is capable of extruding chemotherapeutics outside the cell and its overexpression in certain cancer cells may cause failure of chemotherapy. Many attempts were carried out to identify potent inhibitors of this transporter and numerous compounds were shown to exert inhibitory effects in vitro, but so far none were able to make their way to the clinic due to serious complications. Natural compounds represent a great source of therapeutics, which are believed to be safe and effective. Therefore, we have screened a large library of naturally occurring cardiotonic steroids and their derivatives using high throughput flow cytometry. We were able to identify six compou…

Cell SurvivalHigh-throughput screeningIn silicoPharmacologyBiochemistryProtein Structure SecondaryCell LineFlow cytometryCardiac Glycosideschemistry.chemical_compoundmedicineHumansATP Binding Cassette Transporter Subfamily B Member 1P-glycoproteinPharmacologyDose-Response Relationship Drugbiologymedicine.diagnostic_testResazurinmedicine.diseaseIn vitroProtein Structure TertiaryLeukemiachemistryDoxorubicinCancer cellbiology.proteinBiochemical Pharmacology
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Photoactivation of Anticancer Ru Complexes in Deep Tissue: How Deep Can We Go?

2017

Activation of anticancer therapeutics such as ruthenium (Ru) complexes is currently a topic of intense investigation. The success of phototherapy relies on photoactivation of therapeutics after the light passes through skin and tissue. In this paper, the photoactivation of anticancer Ru complexes with 671-nm red light through tissue of different thicknesses was studied. Four photoactivatable Ru complexes with different absorption wavelengths were synthesized. Two of them (Ru3 and Ru4) were responsive to wavelengths in the “therapeutic window” (650–900 nm) and could be activated using 671-nm red light after passing through tissue up to 16-mm-thick. The other two (Ru1 and Ru2) could not be ac…

Cell SurvivalInfrared Rayschemistry.chemical_elementAntineoplastic Agents02 engineering and technologyAbsorption (skin)010402 general chemistryPhotochemistry01 natural sciencesCatalysisRutheniumMETALLODRUGDeep tissueCoordination ComplexesHumansRed lightPHOTOTHERAPYTherapeutic windowChemistryPHOTOCHEMISTRYOtras Ciencias QuímicasOrganic ChemistryLight activatedCiencias QuímicasGeneral Chemistry021001 nanoscience & nanotechnology0104 chemical sciencesRutheniumRU COMPLEXSpectrophotometryCancer cellANTICANCER0210 nano-technologyCIENCIAS NATURALES Y EXACTASHeLa Cells
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Geldanamycin-induced osteosarcoma cell death is associated with hyperacetylation and loss of mitochondrial pool of heat shock protein 60 (hsp60)

2013

Osteosarcoma is one of the most malignant tumors of childhood and adolescence that is often resistant to standard chemo- and radio-therapy. Geldanamycin and geldanamycin analogs have been recently studied as potential anticancer agents for osteosarcoma treatment. Here, for the first time, we have presented novel anticancer mechanisms of geldanamycin biological activity. Moreover, we demonstrated an association between the effects of geldanamycin on the major heat shock proteins (HSPs) and the overall survival of highly metastatic human osteosarcoma 143B cells. We demonstrated that the treatment of 143B cells with geldanamycin caused a subsequent upregulation of cytoplasmic Hsp90 and Hsp70 w…

Cell SurvivalLactams Macrocycliclcsh:MedicineApoptosisBone NeoplasmsBiologyMitochondrionMitochondrial Proteinschemistry.chemical_compoundGeldanamycin Hsp60 Osteosarcoma cellHeat shock proteinCell Line Tumorpolycyclic compoundsBenzoquinonesHumansHeat shocklcsh:ScienceCell ProliferationOsteosarcomaMultidisciplinaryAntibiotics Antineoplasticlcsh:RAcetylationChaperonin 60GeldanamycinHsp90Molecular biologyMitochondriaProtein TransportchemistryCancer cellCancer researchbiology.proteinApoptotic signaling pathwayHSP60lcsh:QDrug Screening Assays AntitumorProtein Processing Post-TranslationalResearch ArticleSignal Transduction
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Cell cycle arrest and induction of apoptosis by cajanin stilbene acid from Cajanus cajan in breast cancer cells

2015

Abstract Background: The low abundant cajanin stilbene acid (CSA) from Pigeon Pea ( Cajanus cajan ) has been shown to kill estrogen receptor α positive cancer cells in vitro and in vivo . Downstream effects such as cell cycle and apoptosis-related mechanisms have not been analyzed yet. Material and methods: We analyzed the activity of CSA by means of flow cytometry (cell cycle distribution, mitochondrial membrane potential, MMP), confocal laser scanning microscopy (MMP), DNA fragmentation assay (apoptosis), Western blotting (Bax and Bcl-2 expression, caspase-3 activation) as well as mRNA microarray hybridization and Ingenuity pathway analysis. Results: CSA induced G2/M arrest and apoptosis …

Cell cycle checkpointDNA damageCellPharmaceutical ScienceApoptosisBiologyFlow cytometryCajanusStilbenesDrug DiscoverymedicineHumansbcl-2-Associated X ProteinMembrane Potential MitochondrialPharmacologymedicine.diagnostic_testCaspase 3Cell Cycle CheckpointsCell cycleMolecular biologySalicylatesGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Complementary and alternative medicineApoptosisCancer cellMCF-7 CellsMolecular MedicineDNA fragmentationDNA DamageSignal TransductionPhytomedicine
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All-trans retinoic acid restores gap junctional intercellular communication between oral cancer cells with upregulation of Cx32 and Cx43 expressions …

2012

Objective: All-trans retinoic acid (ATRA) has been demonstrated to inhibit tumor growth by restoration of gap junctional intercellular communication (GJIC) via upregulation of connexin (Cx) expression in some solid tumors. However, the relationship between ATRA and GJIC remains unclear in oral squamous cell carcinoma (OSCC). The aim of this study was to investigate the effect of ATRA on the GJIC function of OSCC. Study design: We measured the effects of ATRA on the viability and cell cycle distribution of SCC9 and Tca8113 OSCC cells. The GJIC function was observed using the scrape-loading dye transfer technique, and the mRNA and protein levels of Cx32 and Cx43 were detected by qRT-PCR, West…

Cell cycle checkpointRetinoic acidConnexinAntineoplastic AgentsTretinoinOdontologíaCell CommunicationConnexinschemistry.chemical_compoundDownregulation and upregulationTretinoinmedicineTumor Cells CulturedHumansRNA MessengerGeneral DentistryneoplasmsMouth neoplasmOral Medicine and Pathologyorganic chemicalsGap JunctionsCell cycle:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludbiological factorsUp-RegulationGene Expression Regulation Neoplasticstomatognathic diseasesOtorhinolaryngologychemistryConnexin 43ImmunologyCancer cellUNESCO::CIENCIAS MÉDICASCancer researchCarcinoma Squamous CellSurgeryMouth NeoplasmsResearch-Articlemedicine.drug
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Antitumor effects of curcumin and structurally β-diketone modified analogs on multidrug resistant cancer cells

2007

Abstract Using concepts of bioisostery a series of curcumin analogs were synthesized: the diketonic system of the compound was elaborated into enaminones, oximes, and the isoxazole heterocycle. The cell growth inhibitory and apoptosis inducing effects of the new analogs were evaluated by in vitro assays in the hepatocellular carcinoma HA22T/VGH cells, as well as in the MCF-7 breast cancer cell line and in its multidrug resistant (MDR) variant MCF-7R. Increased antitumor activity on all cell lines was found with the isoxazole analog and especially with the benzyl oxime derivative; in the HA22T/VGH cell model, the latter compound inhibited constitutive NF-κB activation.

Cell growth inhibitionSpectrometry Mass Electrospray IonizationCurcuminMagnetic Resonance SpectroscopyMDR breast cancer cellsClinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsBiochemistrychemistry.chemical_compoundCell Line TumorDrug DiscoveryNF-κB inhibitionHumansIsoxazoleCytotoxicityMolecular BiologyChromatography High Pressure LiquidCell growthOrganic ChemistryCell growth inhibition; Curcumin oxime derivatives; MDR breast cancer cells; NF-κB inhibition;KetonesCurcumin oxime derivativesDrug Resistance MultipleMultiple drug resistancechemistryBiochemistryDrug Resistance NeoplasmCell cultureApoptosisCancer cellSettore BIO/14 - FarmacologiaCurcuminMolecular MedicineCellBioorganic & Medicinal Chemistry Letters
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Cajanol, a novel anticancer agent from Pigeonpea [Cajanus cajan (L.) Millsp.] roots, induces apoptosis in human breast cancer cells through a ROS-med…

2010

Cajanol (5-hydroxy-3-(4-hydroxy-2-methoxyphenyl)-7-methoxychroman-4-one) is an isoflavanone from Pigeonpea [Cajanus cajan (L.) Millsp.] roots. As the most effective phytoalexin in pigeonpea, the cytotoxic activity of cajanol towards cancer cells has not been report as yet. In the present study, the anticancer activity of cajanol towards MCF-7 human breast cancer cells was investigated. In order to explore the underlying mechanism of cell growth inhibition of cajanol, cell cycle distribution, DNA fragmentation assay and morphological assessment of nuclear change, ROS generation, mitochondrial membrane potential (DeltaPsim) disruption, and expression of caspase-3 and caspase-9, Bax, Bcl-2, PA…

Cell growthCytochrome cApoptosisBreast NeoplasmsGeneral MedicineMitochondrionCell cycleBiologyToxicologyFlow CytometryMolecular biologyAntineoplastic Agents PhytogenicIsoflavonesPlant RootsMitochondriaCajanusCell cultureApoptosisCell Line TumorCancer cellbiology.proteinCytotoxic T cellHumansFemaleReactive Oxygen SpeciesChemico-biological interactions
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