Search results for " Neoplastic"

showing 10 items of 662 documents

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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Type V collagen and protein kinase C η down-regulation in 8701-BC breast cancer cells.

2011

We previously reported that ductal infiltrating carcinomas (d.i.c.) of the human breast display profound modifications of the stromal architecture, associated with anomalous collagen composition. Among the major alterations observed in the interstitial collagen, the relative increase of type V collagen content was detected. When type V collagen was used as an ‘‘in vitro’’ substrate for 8701-BC d.i.c. cells, it appeared able to restrain cell growth, inhibit cell motility and invasion ‘‘in vitro’’, and modify the expression levels of genes coding for apoptosis factors, caspases and stress response proteins. In the present paper we demonstrate that type V collagen induces the down-regulation o…

Caspase 8bcl-X ProteinDown-RegulationApoptosisBreast NeoplasmsDNA FragmentationOligonucleotides AntisenseGene Expression Regulation NeoplasticIsoenzymesCaspasesCell Line TumorHumansFemalebcl-Associated Death ProteinSettore BIO/06 - Anatomia Comparata E CitologiaCollagen Type Vdifferential display protein kinase breast cancer gene expression collagenProtein Kinase CCell ProliferationMolecular carcinogenesis
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Colon Cancer Stem Cells: Promise of Targeted Therapy

2010

First developed for hematologic disorders, the concept of cancer stem cells (CSCs) was expanded to solid tumors, including colorectal cancer (CRC). The traditional model of colon carcinogenesis includes several steps that occur via mutational activation of oncogenes and inactivation of tumor suppressor genes. Intestinal epithelial cells exist for a shorter amount of time than that required to accumulate tumor-inducing genetic changes, so researchers have investigated the concept that CRC arises from the long-lived stem cells, rather than from the differentiated epithelial cells. Colon CSCs were originally identified through the expression of the CD133 glycoprotein using an antibody directed…

Cell SurvivalColonColorectal cancermedicine.medical_treatmentMetastasisTargeted therapyColon cancer stem cellsCancer stem cellBiomarkers TumormedicineAnimalsHumansHepatologybiologyCD44GastroenterologyLGR5Cell Differentiationmedicine.diseaseGene Expression Regulation NeoplasticCell Transformation NeoplasticDrug Resistance NeoplasmColonic NeoplasmsNeoplastic Stem CellsCancer researchbiology.proteinStem cellSignal TransductionAdult stem cell
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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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[Post-translational regulation of N-glycosylated proteins expression in human intestinal cells in culture].

1991

International audience; HT-29 cells derived from a human colonic adenocarcinoma, can express a typical intestinal differentiation. Undifferentiated HT-29 cells accumulate N-linked glycoproteins substituted with unprocessed carbohydrate chains before to degrade them. Conversely, carbohydrate chains of N-linked glycoproteins are classically processed in differentiated HT-29 cells. The instability of N-linked glycoproteins in undifferentiated HT-29 cells is due to their rapid delivery from the endoplasmic reticulum to a compartment with lysosomal characteristics. This catabolitic pathway involves a bypass of the Golgi apparatus.

Cell Transformation NeoplasticDrug StabilityLeupeptinsPolysaccharides[ CHIM.ORGA ] Chemical Sciences/Organic chemistry[CHIM.ORGA]Chemical Sciences/Organic chemistryColonic NeoplasmsTumor Cells CulturedHumansAdenocarcinoma[CHIM.ORGA] Chemical Sciences/Organic chemistryProtein Processing Post-TranslationalGlycoproteins
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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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Proliferative activity and tumorigenic conversion: impact on cellular metabolism in 3-D culture

2001

Oxygen consumption, glucose, lactate, and ATP concentrations, as well as glucose and lactate turnover rates, have been studied in a three-dimensional carcinogenesis model of differently transformed rat embryo fibroblasts (spontaneously immortalized Rat1 and myc-transfected M1, and the ras-transfected, tumorigenic descendants Rat1-T1 and MR1) to determine metabolic alterations that accompany tumorigenic conversion. Various bioluminescence techniques, thymidine labeling, measurement of[Formula: see text] distributions with microelectrodes, and determination of cellular oxygen uptake rates (Q˙[Formula: see text]) have been applied. In the ras-transfected, tumorigenic spheroid types, the size d…

Cell divisionPhysiologyBiologymedicine.disease_causeDiffusionchemistry.chemical_compoundAdenosine TriphosphateOxygen ConsumptionSpheroids CellularmedicineAnimalsLactic AcidFibroblastCell Line TransformedCell growthCell BiologyTransfectionFibroblastsEmbryo MammalianRats Inbred F344In vitroRatsLactic acidOxygenCell Transformation NeoplasticGlucosemedicine.anatomical_structurechemistryBiochemistryembryonic structuresCarcinogenesisAdenosine triphosphateCell DivisionAmerican Journal of Physiology-Cell Physiology
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PON3 is upregulated in cancer tissues and protects against mitochondrial superoxide-mediated cell death

2012

To achieve malignancy, cancer cells convert numerous signaling pathways, with evasion from cell death being a characteristic hallmark. The cell death machinery represents an anti-cancer target demanding constant identification of tumor-specific signaling molecules. Control of mitochondrial radical formation, particularly superoxide interconnects cell death signals with appropriate mechanistic execution. Superoxide is potentially damaging, but also triggers mitochondrial cytochrome c release. While paraoxonase (PON) enzymes are known to protect against cardiovascular diseases, recent data revealed that PON2 attenuated mitochondrial radical formation and execution of cell death. Another famil…

Cell signalingProgrammed cell deathMAP Kinase Signaling SystemApoptosisMitochondrionBiologyEndoplasmic ReticulumGene Expression Regulation EnzymologicMicechemistry.chemical_compoundSuperoxidesNeoplasmsAnimalsHumansMolecular BiologyOriginal PaperAryldialkylphosphataseSuperoxideCytochromes cCell BiologyMitochondriaNeoplasm ProteinsUp-RegulationCell biologyGene Expression Regulation NeoplasticHEK293 CellschemistryApoptosisCancer cellDNAJA3Signal transductionCell Death & Differentiation
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p53 as the main traffic controller of the cell signaling network

2010

Among different pathological conditions that affect human beings, cancer has received a great deal of attention primarily because it leads to significant morbidity and mortality. This is essentially due to increasing world-wide incidence of this disease and the inability to discover the cause and molecular mechanisms by which normal human cells acquire the characteristics that define cancer cells. Since the discovery of p53 over a quarter of a century ago, it is now recognized that virtually all cell fate pathways of live cells and the decision to die are under the control of p53. Such extensive involvement indicates that p53 protein is acting as a major traffic controller in the cell signa…

Cell signalingSettore MED/06 - Oncologia MedicaApoptosisDiseaseCell fate determinationBiologyNeoplasmsmedicineApoptosis; Cellular Senescence; Gene Expression Regulation Neoplastic; Humans; Mutation; Neoplasms; Polymorphism Genetic; Signal Transduction; Tumor Suppressor Protein p53HumansCellular SenescencePolymorphism GeneticCancerApoptosiCell cyclemedicine.diseaseCell biologyGene Expression Regulation NeoplasticThe Hallmarks of CancerApoptosisCancer cellMutationNeoplasmTumor Suppressor Protein p53HumanSignal Transduction
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