Search results for "Neoplasms"

showing 10 items of 7988 documents

Betulinic Acid Kills Colon Cancer Stem Cells

2016

Cancer stem cells (CSCs) are considered to be the origin of cancer and it is suggested that they are resistant to chemotherapy. Current therapies fail to eradicate CSCs and therefore selecting a resistant cell subset that is able to facilitate tumor recurrences. Betulinic acid (BetA) is a broad acting natural compound, shown to induce cell death via the inhibition of the stearoyl-CoA- desaturase (SCD- 1). This enzyme converts saturated fatty acids into unsaturated fatty acids and is over-expressed in tumor cells. Here we show that BetA induces rapid cell death in all colon CSCs tested and is able to affect the CSCs directly as shown, via the loss of clonogenic capacity. Similar results were…

0301 basic medicineProgrammed cell deathColorectal cancerMedicine (miscellaneous)Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCancer stem cellBetulinic acidCell Line TumormedicineHumansEnzyme InhibitorsClonogenic assayCell DeathCancer stem cellStearoyl CoA-desaturaseCancerGeneral Medicinemedicine.diseaseBetulinic acidTriterpenesClone CellsColon cancerTumor resistance030104 developmental biologychemistryBiochemistryCell culture030220 oncology & carcinogenesisCancer treatmentColonic NeoplasmsMutationCancer researchNeoplastic Stem CellsStem cellSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioPentacyclic TriterpenesStearoyl-CoA DesaturaseCurrent stem cell research & therapy
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Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.

2017

The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF…

0301 basic medicineProgrammed cell deathLiver tumorCell SurvivalNecroptosisMice TransgenicBiologyChronic liver diseaseProinflammatory cytokine03 medical and health sciencesLiver diseaseMiceLiver Neoplasms ExperimentalmedicineAnimalsDiethylnitrosamineKinase activityTranscription Factor RelAGeneral Medicinemedicine.disease3. Good healthNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticReceptors Tumor Necrosis Factor Type IHepatocyteReceptor-Interacting Protein Serine-Threonine KinasesCancer researchHepatocytesSignal TransductionResearch ArticleThe Journal of clinical investigation
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Anticancer metal drugs and immunogenic cell death

2016

Conventional chemotherapeutics, but also innovative precision anticancer compounds, are commonly perceived to target primarily the cancer cell compartment. However, recently it was discovered that some of these compounds can also exert immunomodulatory activities which might be exploited to synergistically enhance their anticancer effects. One specific phenomenon of the interplay between chemotherapy and the anticancer immune response is the so-called “immunogenic cell death” (ICD). ICD was discovered based on a vaccination effect exerted by cancer cells dying from pretreatment with certain chemotherapeutics, termed ICD inducers, in syngeneic transplantation mouse models. Interestingly, onl…

0301 basic medicineProgrammed cell deathOrganoplatinum Compoundsmedicine.medical_treatmentAntineoplastic AgentsPharmacologyBiochemistryAntineoplastic AgentInorganic ChemistryMice03 medical and health sciences0302 clinical medicineImmune systemCancer immunotherapyNeoplasmsmedicineAnimalsHumansEndoplasmic Reticulum StreCisplatinChemotherapyCell DeathAnimalChemistryOrganoplatinum CompoundEndoplasmic Reticulum Stress3. Good healthOxaliplatin030104 developmental biologyAnticancer metal drugSettore CHIM/03 - Chimica Generale E Inorganica030220 oncology & carcinogenesisCancer cellUnfolded protein responseImmunogenic cell deathCisplatinReactive Oxygen SpecieReactive Oxygen SpeciesImmunogenic cell deathHumanmedicine.drugJournal of Inorganic Biochemistry
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SERCA and P-glycoprotein inhibition and ATP depletion are necessary for celastrol-induced autophagic cell death and collateral sensitivity in multidr…

2019

Multidrug resistance (MDR) represents an obstacle in anti-cancer therapy. MDR is caused by multiple mechanisms, involving ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp), which reduces intracellular drug levels to sub-therapeutic concentrations. Therefore, sensitizing agents retaining effectiveness against apoptosis- or drug-resistant cancers are desired for the treatment of MDR cancers. The sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) pump is an emerging target to overcome MDR, because of its continuous expression and because the calcium transport function is crucial to the survival of tumor cells. Previous studies showed that SERCA inhibitors exhibit anti-c…

0301 basic medicineProgrammed cell deathSERCALung NeoplasmsCell SurvivalAntineoplastic AgentsAutophagy-Related Protein 7Sarcoplasmic Reticulum Calcium-Transporting ATPases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAdenosine TriphosphateCell Line TumorAutophagyAnimalsHumansATP Binding Cassette Transporter Subfamily B Member 1P-glycoproteinPharmacologybiologyDose-Response Relationship DrugChemistryAutophagyXenograft Model Antitumor AssaysDrug Resistance MultipleTriterpenesMultiple drug resistanceMice Inbred C57BL030104 developmental biologyCelastrolApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchHepatocytesPentacyclic TriterpenesPharmacological research
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Viral Bcl2s' transmembrane domain interact with host Bcl2 proteins to control cellular apoptosis

2020

© The Author(s) 2020.

0301 basic medicineProgrammed cell deathScienceProtein domainGeneral Physics and AstronomyApoptosisBiologyVirus-host interactionsArticleGeneral Biochemistry Genetics and Molecular BiologyFluorescenceCell Line03 medical and health sciences0302 clinical medicineProtein Domainsimmune system diseaseshemic and lymphatic diseasesmedicineHumansAmino Acid SequenceAuthor CorrectionPeptide sequenceneoplasmsMultidisciplinaryVirus–host interactionsQCell MembraneGeneral ChemistryViral proteinsmedicine.diseaseControl cellLymphomaCell biologyVirusTransmembrane domain030104 developmental biologyProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisDoxorubicin030220 oncology & carcinogenesisbiological phenomena cell phenomena and immunityProtein MultimerizationHydrophobic and Hydrophilic InteractionsProteïnesProtein Binding
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The HMGB1 protein induces a metabolic type of tumour cell death by blocking aerobic respiration

2016

The high-mobility group box 1 (HMGB1) protein has a central role in immunological antitumour defense. Here we show that natural killer cell-derived HMGB1 directly eliminates cancer cells by triggering metabolic cell death. HMGB1 allosterically inhibits the tetrameric pyruvate kinase isoform M2, thus blocking glucose-driven aerobic respiration. This results in a rapid metabolic shift forcing cells to rely solely on glycolysis for the maintenance of energy production. Cancer cells can acquire resistance to HMGB1 by increasing glycolysis using the dimeric form of PKM2, and employing glutaminolysis. Consistently, we observe an increase in the expression of a key enzyme of glutaminolysis, malic …

0301 basic medicineProgrammed cell deathThyroid HormonesCellular respirationScienceCell RespirationMalic enzymeGeneral Physics and Astronomychemical and pharmacologic phenomenaPKM2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesCell Line TumorHumansGlycolysisHMGB1 ProteinMultidisciplinaryGlutaminolysisCell DeathQMembrane ProteinsGeneral ChemistryCell biology030104 developmental biologyGlucoseCancer cellColonic NeoplasmsCarrier ProteinsGlycolysisPyruvate kinaseNature Communications
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The dissociation of the Hsp60/pro-Caspase-3 complex by bis(pyridyl)oxadiazole copper complex (CubipyOXA) leads to cell death in NCI-H292 cancer cells

2017

Abstract Cell survival and proliferation are central to carcinogenesis, involving various mechanisms among which those that impede apoptosis are important. In this, the role of the molecular chaperone Hsp60 is unclear since it has been reported that it can be both, pro- or anti-apoptotic. A solution to this riddle is crucial to the development of anti-cancer therapies targeting Hsp60. We addressed this question using a tumor cell line, NCI-H292, and [Cu(3,5-bis(2′-pyridyl)-1,2,4-oxadiazole) 2 (H 2 O) 2 ](ClO 4 ) 2 , CubipyOXA , a copper-containing compound with cytotoxic properties. We treated cells with various doses of the compound and measured cell viability; apoptosis indicators; and le…

0301 basic medicineProgrammed cell deathanimal structuresApoptosischemical and pharmacologic phenomenaCaspase 3medicine.disease_causecomplex mixturesBiochemistryMitochondrial ProteinsHsp60/pC3 complexInorganic Chemistry03 medical and health sciences0302 clinical medicineCoordination ComplexesCell Line TumorNeoplasmsCubipyOXAmedicineHumansCytotoxic T cellViability assayCancerOxadiazolesCaspase 3ChemistryfungiApoptosiChaperonin 60Hsp60Neoplasm ProteinsCell biology030104 developmental biologyApoptosisPro-caspase-3 (pC3)Multiprotein Complexes030220 oncology & carcinogenesisCancer cellHSP60Apoptosis; Cancer; CubipyOXA; Hsp60; Hsp60/pC3 complex; Pro-caspase-3 (pC3); Biochemistry; Inorganic ChemistryCarcinogenesisCopper
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Sicilian Litchi Fruit Extracts Induce Autophagy versus Apoptosis Switch in Human Colon Cancer Cells

2018

Litchi chinensis Sonnerat is a tropical tree whose fruits contain significant amounts of bioactive polyphenols. Litchi cultivation has recently spread in Sicily where the climate conditions are particularly favorable for this crop. Recent findings have shown that Litchi extracts display anti-tumor and pro-apoptotic effects in vitro, but the precise underlying mechanisms have not been fully elucidated. In this study, we report for the first time the effects of Sicilian litchi fruit extracts on colon cancer cells. The results indicated that litchi exocarp, mesocarp and endocarp fractions reduce the viability and clonogenic growth of HT29 cells. These effects were due to cell cycle arrest in t…

0301 basic medicineProgrammed cell deathautophagyCell cycle checkpointAtg1Apoptosislcsh:TX341-641Litchi chinensisArticle03 medical and health sciencesHT29 Cells0302 clinical medicineLitchiSettore BIO/10 - BiochimicaHumansClonogenic assaySicilyNutrition and DieteticsPlant ExtractsChemistryKinaseAutophagyPolyphenolsLitchi chinensiCell Cycle CheckpointsAntineoplastic Agents PhytogenicCell biology030104 developmental biologycolon cancerApoptosisFruit030220 oncology & carcinogenesisColonic Neoplasmsanti-tumor activityCaco-2 Cells<i>Litchi chinensis</i>HT29 Cellslcsh:Nutrition. Foods and food supplyPhytotherapySignal TransductionFood ScienceNutrients
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Protease‐activated receptor signaling in intestinal permeability regulation

2019

Protease-activated receptors (PARs) are a unique class of G-protein-coupled transmembrane receptors, which revolutionized the perception of proteases from degradative enzymes to context-specific signaling factors. Although PARs are traditionally known to affect several vascular responses, recent investigations have started to pinpoint the functional role of PAR signaling in the gastrointestinal (GI) tract. This organ is exposed to the highest number of proteases, either from the gut lumen or from the mucosa. Luminal proteases include the host's digestive enzymes and the proteases released by the commensal microbiota, while mucosal proteases entail extravascular clotting factors and the enzy…

0301 basic medicineProteasesCell typeProtease-activated receptorReceptors Proteinase-ActivatedBiologyBiochemistryPermeabilityEpitheliumInflammatory bowel disease03 medical and health sciencesGastrointestinal cancer0302 clinical medicineImmune systemmedicineAnimalsHumansProtease-activated receptorIntestinal MucosaSymbiosisReceptorMolecular BiologyMicrobial proteasesGastrointestinal NeoplasmsClotting factorIntestinal permeabilityCoagulationMicrobiotaEpithelial barrier functionCell BiologyInflammatory Bowel Diseasesmedicine.diseaseIntestinal epitheliumTissue factorGastrointestinal MicrobiomeCell biologyIntestineGastrointestinal TractDisease Models Animal030104 developmental biologyGene Expression RegulationBacterial Translocation030220 oncology & carcinogenesisPeptide HydrolasesSignal Transduction
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Lunasin is a redox sensitive intrinsically disordered peptide with two transiently populated α-helical regions.

2016

Lunasin is a 43 amino acid peptide with anti-cancer, antioxidant, anti-inflammatory and cholesterol-lowering properties. Although the mechanism of action of lunasin has been characterized to some extent, its exact three-dimensional structure as well as the function of the N-terminal sequence remains unknown. We established a novel method for the production of recombinant lunasin that allows efficient isotope labeling for NMR studies. Initial studies showed that lunasin can exist in a reduced or oxidized state with an intramolecular disulfide bond depending on solution conditions. The structure of both forms of the peptide at pH 3.5 and 6.5 was characterized by CD spectroscopy and multidimen…

0301 basic medicineProtein Conformation alpha-HelicalCircular dichroismPhysiologyBeta sheetPeptideIntrinsically disordered proteinsBiochemistryLunasinAntioxidantsHistones03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineEndocrinologyNeoplasmsAnticarcinogenic AgentsHumansAmino Acid SequenceDisulfidesProtein secondary structureNuclear Magnetic Resonance BiomolecularPlant Proteinschemistry.chemical_classificationChemistryAcetylationNuclear magnetic resonance spectroscopyIntrinsically Disordered Proteins030104 developmental biologyBiochemistry030220 oncology & carcinogenesisBiophysicsSoybean ProteinsPeptidesOxidation-ReductionFunction (biology)Peptides
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