Search results for "Neoplastic"

showing 10 items of 2901 documents

WIN55,212-2-induced expression of Mir-29b1 favours the suppression of osteosarcoma cell migration in a SPARC-independent manner

2019

WIN55,212-2 (WIN) is a synthetic agonist of cannabinoid receptors that displays promising antitumour properties. The aim of this study is to demonstrate that WIN is able to block the migratory ability of osteosarcoma cells and characterize the mechanisms involved. Using wound healing assay and zymography, we showed that WIN affects cell migration and reduces the activity of the metalloproteases MMP2 and MMP9. This effect seemed to be independent of secreted protein acidic and rich in cysteine (SPARC), a matricellular protein involved in tissue remodeling and extracellular matrix deposition. SPARC release was indeed prevented by WIN, and SPARC silencing by RNA interference did not influence …

Cannabinoid receptorMorpholinesAntineoplastic AgentsMMP9NaphthalenesCatalysisArticlelcsh:ChemistryInorganic ChemistryExtracellular matrixExtracellular VesiclescannabinoidsDownregulation and upregulationCell MovementCell Line TumorSettore BIO/10 - BiochimicaGene silencingHumansOsteonectinCell migrationPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyCannabinoidSpectroscopyCell ProliferationOsteosarcomaChemistryCell growthOrganic ChemistryMatricellular proteinCell migrationSPARCGeneral MedicineComputer Science ApplicationsCell biologyBenzoxazinesMiR-29b1MicroRNAslcsh:Biology (General)lcsh:QD1-999
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Increased endocannabinoid levels reduce the development of precancerous lesions in the mouse colon

2007

Colorectal cancer is an increasingly important cause of death in Western countries. Endocannabinoids inhibit colorectal carcinoma cell proliferation in vitro. In this paper, we investigated the involvement of endocannabinoids on the formation of aberrant crypt foci (ACF, earliest preneoplastic lesions) in the colon mouse in vivo. ACF were induced by azoxymethane (AOM); fatty acid amide hydrolase (FAAH) and cannabinoid receptor messenger ribonucleic acid (mRNA) levels were analyzed by the quantitative reverse transcription polymerase chain reaction (RT-PCR); endocannabinoid levels were measured by liquid chromatography-mass spectrometry; caspase-3 and caspase-9 expressions were measured by W…

Cannabinoid receptormedicine.medical_treatment2-Arachidonoylglycerolpreneoplastic lesionsMass Spectrometrychemistry.chemical_compoundMice0302 clinical medicineFatty acid amide hydrolaseDrug DiscoveryFatty acid amide hydrolase (FAAH)Aberrant crypt fociGenetics(clinical)ReceptorReceptors CannabinoidGenetics (clinical)Medicine(all)0303 health sciencesCaspase 3Reverse Transcriptase Polymerase Chain ReactionEndocannabinoid systemCaspase 93. Good health2-arachidonoylglycerolColon cancer030220 oncology & carcinogenesisColonic NeoplasmsMolecular Medicinelipids (amino acids peptides and proteins)psychological phenomena and processesRapid CommunicationAberrant crypt focimedicine.medical_specialtyColonAzoxymethaneBiologydigestive systemAmidohydrolases03 medical and health sciencesInternal medicineCannabinoid Receptor ModulatorsmedicineAnimalsRNA MessengerCannabinoid receptors030304 developmental biologyAzoxymethaneendocannabinoiddigestive system diseasesEndocrinologychemistrynervous systemCancer researchCannabinoidcancer pharmacologyPrecancerous ConditionsEndocannabinoids
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Phylostratic Shift of Whole-Genome Duplications in Normal Mammalian Tissues towards Unicellularity Is Driven by Developmental Bivalent Genes and Reve…

2020

Tumours were recently revealed to undergo a phylostratic and phenotypic shift to unicellularity. As well, aggressive tumours are characterized by an increased proportion of polyploid cells. In order to investigate a possible shared causation of these two features, we performed a comparative phylostratigraphic analysis of ploidy-related genes, obtained from transcriptomic data for polyploid and diploid human and mouse tissues using pairwise cross-species transcriptome comparison and principal component analysis. Our results indicate that polyploidy shifts the evolutionary age balance of the expressed genes from the late metazoan phylostrata towards the upregulation of unicellular and early m…

CarcinogenesisCircadian clockAntineoplastic AgentsBiologyGenomeArticleCatalysisBivalent (genetics)Epigenesis Geneticlcsh:ChemistryProto-Oncogene Proteins c-mycInorganic ChemistryTranscriptomeMicePolyploidGene DuplicationNeoplasmsProtein Interaction MappingAnimalsHumanscancerEpigeneticsPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyGenepolyploidybivalent genesSpectroscopyGeneticsGenomePloidiesCircadian Rhythm Signaling Peptides and ProteinsOrganic Chemistryearly multicellularityviral-origin oncogenesOncogenesGeneral MedicineembryonalityPhenotypeNeoplasm ProteinsunicellularityComputer Science ApplicationsGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999Drug Resistance NeoplasmMetabolic Networks and PathwaysInternational Journal of Molecular Sciences
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Cyclooxygenases in hepatocellular carcinoma

2006

Many epidemiological studies demonstrate that treatment with non-steroidal anti-inflammatory drugs (NSAIDs) reduce the incidence and mortality of certain malignancies, especially gastrointestinal cancer. The cyclooxygenase (COX) enzymes are well-known targets of NSAIDs. However, conventional NSAIDs non-selectively inhibit both the constitutive form COX-1, and the inducible form COX-2. Recent evidence indicates that COX-2 is an important molecular target for anticancer therapies. Its expression is undetectable in most normal tissues, and is highly induced by pro-inflammatory cytokines, mitogens, tumor promoters and growth factors. It is now well-established that COX-2 is chronically overexpr…

Carcinoma HepatocellularAngiogenesisBiologymedicine.disease_causeModels BiologicalGene Expression Regulation EnzymologicIn vivomedicineHumansNeoplasm InvasivenessGastrointestinal cancerEnzyme InhibitorsCell growthAnti-Inflammatory Agents Non-SteroidalLiver NeoplasmsGastroenterologyGeneral MedicineHCCSmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticEditorialModels ChemicalCyclooxygenase 2Hepatocellular carcinomaImmunologyCyclooxygenase 1Cancer researchCarcinogenesisLiver cancer
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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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Analysis of Possible Mechanisms Accounting for Raf-1 Kinase Inhibitor Protein Downregulation in Hepatocellular Carcinoma

2012

Abstract Raf-1 kinase inhibitor protein (RKIP) is a tumor and metastasis suppressor that promotes drug-induced apoptosis in cancer cells. It is frequently downregulated, both at the mRNA and protein level, in hepatocellular carcinoma (HCC), but the mechanisms leading to this reduction are obscure. We sequenced the whole RKIP gene in three human HCC cell lines (HA22T/VGH, HepG2, and Hep3B), and in five clinical HCC samples, but could not find any gene variant that might account for their low RKIP levels. We also examined whether gene methylation may be responsible for the altered RKIP expression. No methylation of the RKIP gene was found in the tumor samples, while among the cell lines only …

Carcinoma HepatocellularLeupeptinsAntineoplastic AgentsPhosphatidylethanolamine Binding ProteinRKIP (Raf-1 kinase inhibitor protein) hepatocellular carcinomaBiologyBiochemistryDownregulation and upregulationRNA interferenceCell Line TumorGeneticsHumansMetastasis suppressorPromoter Regions GeneticMolecular BiologyRegulation of gene expressionKinaseLiver NeoplasmsHep G2 CellsMethylationDNA Methylationdigestive system diseasesGene Expression Regulation NeoplasticMicroRNAsMutationCancer cellDNA methylationAzacitidineSettore BIO/14 - FarmacologiaCancer researchMolecular MedicineRNA InterferenceBiotechnologyOMICS: A Journal of Integrative Biology
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Collecting evidence for a stem cell hypothesis in HCC.

2010

Ever since Ernest McCulloch and James E Till defined essential stem cell properties, the field of stem cell biology has attracted increasing interest.1 Manipulating embryonic stem cells has resulted in advanced genetic technologies such as knock-out and transgenic animals, providing valuable models to study genetic influence on a wide variety of diseases.2 The success in manipulating stem cells and the ability to differentiate them into diverse tissues brought with them countless concepts of utilising stem cells in medicine. The idea of perpetually dividing pluripotent cells, capable of differentiating into nearly every possible cell or tissue type, seems like an inexhaustible resource for …

Carcinoma HepatocellularStem cell theory of agingLiver NeoplasmsGastroenterologyClinical uses of mesenchymal stem cellsBiologyEmbryonic stem cellCell biologyRecurrenceImmunologyBiomarkers TumorNeoplastic Stem CellsHumansStem cellProgenitor cellInduced pluripotent stem cellAdult stem cellStem cell transplantation for articular cartilage repairGut
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Molecular diagnosis and therapy of hepatocellular carcinoma (HCC): an emerging field for advanced technologies.

2011

Despite great progress in diagnosis and management of hepatocellular carcinoma (HCC), the exact biology of the tumor remains poorly understood overall limiting the patients' outcome. Detailed analysis and characterization of the molecular mechanisms and subsequently individual prediction of corresponding prognostic traits would revolutionize both diagnosis and treatment of HCC and is the key goal of modern personalized medicine. Over the recent years systematic approaches for the analysis of whole tumor genomes and transcriptomes as well as epigenomes became affordable tools in translational research. This includes simultaneous analyses of thousands of molecular targets using microarray-bas…

Carcinoma HepatocellularSystems biologyGenomicsTranslational researchDiseaseBioinformaticsTarget therapyEpigenesis GeneticTranslational Research BiomedicalCancer stem cellmedicineHumansMolecular pathogenesisPathology MolecularHepatologybusiness.industrySystems BiologyLiver NeoplasmsGenomicsGene expression profilemedicine.diseaseHepatocellular carcinomaNeoplastic Stem CellsPersonalized medicineLiver cancerbusinessTranscriptomeLiver cancerSignal TransductionJournal of hepatology
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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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Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardioto…

2015

Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal model…

Cardiac function curveACE inhibitorsCardiotonic AgentsNeuregulin-1CardiomyopathyAntineoplastic AgentsPreclinical modelsCardioprotectionCardiotonic AgentsPharmacologyBioinformaticsmedicine.disease_causeCancer therapy-induced cardiac injury ;Preclinical modelsMitochondria HeartBeta-blockersNeoplasmsCancer therapy-induced cardiac injuryMedicineAnimalsHumansCardiac stem cellsCardioprotectionCardiotoxicityACE inhibitors; Beta-blockers; Cancer therapy-induced cardiac injury; Cardiac stem cells; Cardioprotection; Mitochondria; Neuregulin-1; Oxidative stress; Preclinical models; Statinsbusiness.industryStatinsCancermedicine.diseaseCardiotoxicityMitochondriaCancer therapy-induced cardiac injury Preclinical models Cardioprotection Mitochondria Neuregulin-1 Oxidative stress Statins Beta-blockers ACE inhibitors Cardiac stem cellsDisease Models AnimalOxidative StressHeart failureCardiology and Cardiovascular MedicinebusinessOxidative stress
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