Search results for "Apoptosi"

showing 10 items of 1846 documents

Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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Cannabinoid-associated cell death mechanisms in tumor models (review)

2012

In recent years, cannabinoids (the active components of Cannabis sativa) and their derivatives have received considerable interest due to findings that they can affect the viability and invasiveness of a variety of different cancer cells. Moreover, in addition to their inhibitory effects on tumor growth and migration, angiogenesis and metastasis, the ability of these compounds to induce different pathways of cell death has been highlighted. Here, we review the most recent results generating interest in the field of death mechanisms induced by cannabinoids in cancer cells. In particular, we analyze the pathways triggered by cannabinoids to induce apoptosis or autophagy and investigate the in…

Cannabinoids apoptosis autophagy synergistic effectsSettore BIO/10 - Biochimica
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Capsaicin Intake and Oral Carcinogenesis: a Systematic Review

2021

Background Chili is the most heavily and frequently consumed spice, either as a flavouring or colouring agent, and it is also a major source of pro-vitamin A, vitamin E and C. The main capsinoidcapsaicinoid found in chili peppers is capsaicin. It has been demonstrated that capsaicin acts as a cancer-suppressing agent through its antioxidant and anti-inflammatory effects, by blocking several signal transduction pathways. Oral squamous cell carcinoma is one of the most prevalent cancer worldwide. It is noteworthy that in countries where populations of diverse ethnic groups co-exist, differences have been observed in terms of incidence of oral cancer. The variances in their diet could explain,…

Carcinogenesismedicine.medical_treatmentpiezosurgeryoral epithelial clysplasiaReviewCapsicum-Annuum LResveratrolPharmacologyresveratrolmedicine.disease_causecapsaicintrismuschemistry.chemical_compoundpreventionHumansMedicinecancerpainGeneral DentistryUNESCO:CIENCIAS MÉDICASOral Medicine and Pathologybusiness.industryCell growthVitamin EIncidence (epidemiology)apoptosisCancerchilioral cancermedicine.diseaseimpacted third molarinhibitioncell proliferationOtorhinolaryngologychemistryCapsaicinApoptosischili-pepperCarcinoma Squamous CellcellsMouth NeoplasmsSurgeryCapsicumbusinessCarcinogenesisedemametabolism
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Cytotoxicity of oleanolic and ursolic acid derivatives toward hepatocellular carcinoma and evaluation of NF-κB involvement.

2019

Oleanolic and ursolic acids are two ubiquitous isomeric triterpene phytochemicals known for their anticancer activity. A set of derivatives of the two compounds with a modified oxidation state and lipophylicity at C-3 and C-28 positions, were prepared and tested as anticancer agents versus the lines HepG2, Hep3B and HA22T/VGH of hepatocarcinoma, a strongly aggressive tumor that is not responsive toward the standard therapies. New derivatives containing a three carbons side chain on the C-3 position were synthetized in both stereoisomeric forms by the Barbier-Grignard procedure and three of them were found to be active toward all of the three targets. The implication of the transcriptional n…

Carcinoma HepatocellularApoptosis01 natural sciencesBiochemistrychemistry.chemical_compoundUrsolic acid Oleanolic acid HepG2 Hep3B HA22T/VGH Antitumor activity NF−κBUrsolic acidTriterpeneOleaDrug DiscoverymedicineTumor Cells CulturedHumansSettore BIO/15 - Biologia FarmaceuticaOleanolic AcidCytotoxicityMolecular BiologyCell Proliferationchemistry.chemical_classification010405 organic chemistryPlant ExtractsOrganic ChemistryLiver NeoplasmsNF-kappa BNF-κBSettore CHIM/06 - Chimica Organicamedicine.diseaseAntineoplastic Agents Phytogenicdigestive system diseasesTriterpenes0104 chemical sciences010404 medicinal & biomolecular chemistrychemistryMechanism of actionHepatocellular carcinomaMalusSettore BIO/14 - FarmacologiaCancer researchmedicine.symptomBioorganic chemistry
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Aspidin PB, a phloroglucinol derivative, induces apoptosis in human hepatocarcinoma HepG2 cells by modulating PI3K/Akt/GSK3β pathway.

2012

Aspidin PB, a phloroglucinol derivative isolated from Dryopteris fragrans (L.) Schott, has been previously reported to exert high biological activities. In the present study, we analyzed the apoptotic mechanisms of aspidin PB on human hepatoma cell line, HepG2. Initially, aspidin PB was shown to inhibit the growth of HepG2 cells in a time and dose-dependent manner. After treatment with aspidin PB for 72 h, 48 h and 24 h using MTT assay, the IC(50) values were 10.59 μM, 20.86 μM and 46.59 μM, respectively. Aspidin PB was capable to induce apoptosis, as measured by mitochondrial membrane potential (ΔΨm), acridine orange (AO) staining and propidium iodide (PI)/annexin V-FITC double staining. T…

Carcinoma HepatocellularApoptosisBiologyPhloroglucinolToxicologyWortmanninchemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesAnnexinHumansMTT assayPropidium iodideProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationPhosphoinositide-3 Kinase InhibitorsMembrane Potential MitochondrialGlycogen Synthase Kinase 3 betaMicroscopy ConfocalAcridine orangeLiver NeoplasmsGeneral MedicineHep G2 CellsFlow CytometryMolecular biologyAndrostadieneschemistryApoptosisWortmanninProto-Oncogene Proteins c-aktSignal TransductionChemico-biological interactions
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Expression of IAPs and alternative splice variants in hepatocellular carcinoma tissues and cells.

2005

IAPs (inhibitors of apoptosis proteins) might have a major role in the apoptotic resistance that marks many cancers. The studies on IAPs in human HCC have focused on survivin or XIAP, indicating that their new or increased expression in this tumor is associated with a more unfavorable prognosis. The present results corroborate these findings, emphasizing the role that the coordinated expression of different IAPs and alternative splice variants might play in the adverse biology of hepatocellular carcinoma.

Carcinoma HepatocellularApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyBioinformaticsGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceCell Line TumorSurvivinCarcinomamedicineHumansspliceRNA MessengerCell ProliferationCell growthReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceAlternative splicingLiver NeoplasmsIntracellular Signaling Peptides and ProteinsProteinsmedicine.diseasePrognosisXIAPbody regionsAlternative SplicingApoptosisDrug Resistance NeoplasmHepatocellular carcinomaCancer researchAnnals of the New York Academy of Sciences
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The Synthetic Cannabinoid WIN 55,212-2 Sensitizes Hepatocellular Carcinoma Cells to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-I…

2010

In this article, we demonstrate that the synthetic cannabinoid R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)-(1-naphthalenyl) methanone mesylate (WIN 55,212-2) sensitizes human hepatocellular carcinoma (HCC) cells to apoptosis mediated by tumor necrosis-related apoptosis inducing ligand (TRAIL). The apoptotic mechanism induced by treatment with WIN/TRAIL combination involved the loss of the mitochondrial transmembrane potential and led to the activation of caspases. In HCC cells, WIN treatment induced the up-regulation of TRAIL death receptor DR5, an effect that seemed to be related to the increase in the level of p8 and CHOP, two factors implicat…

Carcinoma HepatocellularDNA ComplementaryMorpholinesApoptosisNaphthalenesCHOPMembrane PotentialsTNF-Related Apoptosis-Inducing LigandCell Line TumorSurvivinmedicineHumansWIN 55212-2Protein kinase BTranscription factorCaspaseDNA PrimersPharmacologybiologyCannabinoidsReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsGene AmplificationDNA NeoplasmFlow CytometryBenzoxazinesReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMitochondrial MembranesImmunologybiology.proteinCancer researchMolecular MedicineTumor necrosis factor alphaTranscription Factor CHOPmedicine.drugMolecular Pharmacology
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Induction of apoptosis and inhibition of cell growth in human hepatocellular carcinoma cells by COX-2 inhibitors

2005

The aim of the present study was to examine the effects of nonselective (indomethacin) and selective cyclooxygenase-2 (COX-2) inhibitors (NS-398, nimesulide, and CAY10404) on cell growth, cell cycle distribution, and apoptosis in three human hepatocellular carcinoma cell lines (HepG2, HuH-6, and HA22T/VGH) with different characteristics of differentiation and biological behavior. The four COX inhibitors showed a dose-dependent growth-inhibitory effect in all the cell lines. No substantial arrests in the progression of the cells through the cell cycle were observed after treatment of HuH-6 or HA22T/VGH for 48 h with the various inhibitors. On the other hand, there were significant increases …

Carcinoma HepatocellularTime FactorsApoptosisPharmacologyBiologyGeneral Biochemistry Genetics and Molecular BiologyFlow cytometryInhibitory Concentration 50History and Philosophy of ScienceCell Line TumorCarcinomamedicineHumansProtein IsoformsCyclooxygenase InhibitorsEnzyme InhibitorsCell ProliferationCyclooxygenase 2 InhibitorsDose-Response Relationship DrugNeovascularization Pathologicmedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionCell growthGeneral NeuroscienceAnti-Inflammatory Agents Non-SteroidalCell CycleMembrane Proteinsantineoplastic activity apoptosis cancer cell cultureCell cycleFlow Cytometrymedicine.diseaseCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesCell cultureApoptosisHepatocellular carcinomaNimesulidemedicine.drug
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Expression of WISPs and of their novel alternative variants in human hepatocellular carcinoma cells

2005

WISPs (Wnt-induced secreted proteins) are members of the CCN (CTGF/Cyr61/Nov) family involved in fibrotic disorders and tumorigenesis. They have a typical structure composed of four conserved cysteine-rich modular domains, but variants of CCN members lacking one or more modules, generated by alternative splicing or gene mutations, have been described in various pathological conditions. WISP genes were first described as downstream targets of the Wnt signaling pathway, which is frequently altered in human hepatocellular carcinoma (HCC). In the present study, WISP mRNA expression was analyzed by RT-PCR in four human HCC cell lines (HepG2, HuH-6, HuH-7, HA22T/VGH). Our results show for the fir…

Carcinoma HepatocellularWISPHepatocellular carcinomaApoptosisGene mutationBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCCN Intercellular Signaling ProteinsWntalternative splicingHistory and Philosophy of ScienceCell Line TumorProto-Oncogene ProteinsCCN Intercellular Signaling ProteinsmedicineHumansRNA MessengerGeneDNA PrimersOncogene ProteinsGeneticsCCNModels GeneticReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceLiver NeoplasmsAlternative splicingIntracellular Signaling Peptides and ProteinsWnt signaling pathwaydigestive system diseasesNeoplasm ProteinsInsulin-Like Growth Factor Binding ProteinsRepressor ProteinsCTGFCYR61Cancer researchIntercellular Signaling Peptides and ProteinsRNACarcinogenesisWISPWntTranscription Factors
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Oral squamous cell carcinoma and biological markers:an update on the molecules mainly involved in oral carcinogenesis

2007

Squamous cell carcinoma (SCC) is one of the most common malignant cancer of the oral cavity encompassing at least 92.8% of all oral malignancies. Despite improved diagnostic and therapeutic methods over the 20 last years, this tumour is still characterized by a high rate of mortality. The latest advances of molecular biological methods have contributed to better understand the mechanisms involved in the oral carcinogenetic process. Deregulation of cell cycle, apoptosis and cell-cell/cell-matrix adhesions are considered the pathways mainly influencing this multistage event and scientific researches over the last decade have been performed in order to investigate the biological diagnostic and…

Carcinoma Squamous CellCell AdhesionHumansApoptosisMouth Neoplasmsn
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