Search results for "cell growth"

showing 10 items of 662 documents

Resveratrol-mediated apoptosis of hodgkin lymphoma cells involves SIRT1 inhibition and FOXO3a hyperacetylation

2012

Resveratrol (RSV), a plant-derived stilbene, induces cell death in Hodgkin lymphoma (HL)-derived L-428 cells in a dose-dependent manner (IC50 = 27 μM, trypan blue exclusion assay). At a lower range (25 μM), RSV treatment for 48 hr causes arrest in the S-phase of the cell cycle, while at a higher concentration range (50 μM), apoptosis can be detected, with activation of caspase-3. The histone/protein deacetylase SIRT1 has been described as a putative target of RSV action in other model systems, even though its role in cancer cells is still controversial. Here we show that RSV, at both concentration ranges, leads to a marked increase in p53, while a decrease of SIRT1 expression level, as well…

Cancer ResearchPathologymedicine.medical_specialtyProgrammed cell deathApoptosisCell Growth ProcessesBiologyS PhaseSirtuin 1Cell Line TumorStilbenesmedicineHumansbcl-2-Associated X ProteinB-LymphocytesDose-Response Relationship DrugCaspase 3Mantle zoneForkhead Box Protein O3Germinal centerAcetylationForkhead Transcription FactorsCell cycleGerminal CenterHodgkin DiseaseMolecular biologyOncologyResveratrolCell cultureApoptosisCancer cellLymph NodesLymphTumor Suppressor Protein p53International Journal of Cancer
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Cancer-cell traffic in the liver. I. Growth kinetics of cancer cells after portal-vein delivery

1992

Following the intrasplenic injection of B16F10 melanoma cells into mice, at first single cells, and later multicellular tumor foci were observed at different times in the liver. Cell numbers and tumor volumes were determined over the next 12 days, by confocal microscopy of thick liver sections. Fifteen minutes after injection, approximately 20% of the melanoma cells were identified in the liver microvasculature; after 48 hr, only 0.68% of these retained morphologic integrity; by 5 days only 0.13% of the originally detected cells incorporated BUdR; and, by 12 days, these subsequently grew into tumor nodules. Tumor volume changes with time were not exponential and, following a non-replicative…

Cancer ResearchPathologymedicine.medical_specialtyTime FactorsPopulationMelanoma ExperimentalMetastasisMiceMesenteric VeinsParenchymaAnimalsMedicineeducationeducation.field_of_studyPortal Veinbusiness.industryCell growthMelanomaLiver Neoplasmsmedicine.diseaseExtravasationMice Inbred C57BLTransplantationOncologySplenic VeinInjections IntravenousCancer cellFemalebusinessCell DivisionNeoplasm TransplantationInternational Journal of Cancer
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Intestinal epithelial HuR modulates distinct pathways of proliferation and apoptosis and attenuates small intestinal and colonic tumor development.

2014

Abstract HuR is a ubiquitous nucleocytoplasmic RNA-binding protein that exerts pleiotropic effects on cell growth and tumorigenesis. In this study, we explored the impact of conditional, tissue-specific genetic deletion of HuR on intestinal growth and tumorigenesis in mice. Mice lacking intestinal expression of HuR (Hur IKO mice) displayed reduced levels of cell proliferation in the small intestine and increased sensitivity to doxorubicin-induced acute intestinal injury, as evidenced by decreased villus height and a compensatory shift in proliferating cells. In the context of Apcmin/+ mice, a transgenic model of intestinal tumorigenesis, intestinal deletion of the HuR gene caused a three-fo…

Cancer ResearchPost-translational regulationRNA-binding proteinContext (language use)ApoptosisCell Growth ProcessesBiologymedicine.disease_causeArticleAU-rich RNAMiceGene expressionIntestinal NeoplasmsmedicineAnimalsmRNA stabilityIntestinal MucosaMice KnockoutCell growthMolecular biologyPhenotypeProtein-RNA interactionSmall intestineDisease Models Animalmedicine.anatomical_structureOncologyELAV ProteinsApoptosisColonic NeoplasmsCancer researchCarcinogenesis
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In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.

2003

In BCR-ABL-positive cells, the transcription factor STAT-5 is constitutively activated by tyrosine phosphorylation. STAT-5 activation results in upregulation of bcl-X(L) and increased resistance to induction of apoptosis. Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells. Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts. In contrast to JAK-2 and PI-3-kinase inhibition, exposure of K562 cells to imatinib mesylate resulted in obvious suppression of proliferation. R…

Cancer ResearchProgrammed cell deathBlotting WesternFusion Proteins bcr-ablDown-RegulationAntineoplastic AgentsApoptosisBiologyPiperazineschemistry.chemical_compoundDownregulation and upregulationhemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineIn Situ Nick-End LabelingSTAT5 Transcription FactorHumansEnzyme InhibitorsPhosphorylationCell growthCytarabineImatinibTyrosine phosphorylationDrug SynergismHematologyDNAU937 CellsProtein-Tyrosine KinasesMilk ProteinsPrecipitin TestsDNA-Binding ProteinsImatinib mesylatePyrimidinesOncologychemistryApoptosisCaspasesBenzamidesCancer researchImatinib MesylateTrans-ActivatorsTyrosinePoly(ADP-ribose) PolymerasesK562 CellsCell Divisionmedicine.drugK562 cellsSignal TransductionLeukemia
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IFN-alpha-induced apoptosis in hepatocellular carcinoma involves promyelocytic leukemia protein and TRAIL independently of p53.

2009

Abstract IFNs are pleiotropic cytokines that have been shown to be important regulators of cell growth. IFN-α has recently been recognized to harbor therapeutic potential in prevention and treatment of hepatocellular carcinoma (HCC). However, HCC cells respond differentially to IFN treatment, the mechanism of which is largely unknown. To address this issue, we analyzed the effect of IFN-α on different liver tumor cell lines. We found that growth inhibiting effects of IFN-α in hepatoma cells require PML-NB induction and, moreover, tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) expression on the mRNA and protein level. RNAi silencing of PML down-regulates TRAIL expression in …

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTumor suppressor genemedicine.medical_treatmentApoptosisPromyelocytic Leukemia ProteinTNF-Related Apoptosis-Inducing LigandPromyelocytic leukemia proteinMiceCell Line TumormedicineGene silencingAnimalsHumansRNA MessengerbiologyCell growthTumor Suppressor ProteinsLiver NeoplasmsInterferon-alphaNuclear ProteinsCytokineOncologyApoptosisbiology.proteinCancer researchTumor necrosis factor alphaRNA InterferenceTumor Suppressor Protein p53Transcription FactorsCancer research
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Three-dimensional cell culture induces novel proliferative and metabolic alterations associated with oncogenic transformation

1996

To date, cell biological characteristics of oncogene-transfected cells have been investigated either in relatively homogeneous monolayer cultures or in heterogeneous tumors in vivo. To evaluate the emergence of cellular heterogeneity during tumor formation, we have established a multicellular spheroid system from an oncogene-dependent, genetically determined 2-stage carcinogenesis model for 3-dimensional growth under well-defined conditions. The effect of T24Ha-ras transfection on cellular growth, proliferation, cell viability and oxygenation was investigated using spontaneously immortalized (Rat1) and c-myc-transfected (M1) Fisher 344 rat embryo fibroblasts and a tumorigenic T24Ha-ras-tran…

Cancer ResearchProgrammed cell deathCell growthCellTransfectionBiologymedicine.disease_causeCell biologymedicine.anatomical_structureOncologyCell quiescenceCell cultureembryonic structuresImmunologymedicineViability assayCarcinogenesisInternational Journal of Cancer
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2-Triazenoazaindoles: Α novel class of triazenes inducing transcriptional down-regulation of EGFR and HER-2 in human pancreatic cancer cells

2012

Pancreatic cancer is a complex malignancy arising from the accumulation of genetic and epigenetic defects in the affected cells. Standard chemotherapy for patients with advanced disease shows only modest effects and is associated with considerable toxicity. Overexpression or aberrant activation of members of the epidermal growth factor receptor tyrosine kinase family, which includes EGFR and HER-2, occurs frequently and is associated with multiple drug resistance and decreased patient survival. In this study, we have investigated the therapeutic potential of AS104, a novel compound of the triazene class, with potential inhibitory effects on EGFR. We found that treatment of cells with AS104 …

Cancer ResearchProgrammed cell deathmedicine.medical_specialtyIndolesReceptor ErbB-2EGFRCellpancreatic cancer2-triazenoazaindoles pancreatic cancer cell death EGFR HER-2Down-RegulationApoptosisCell Growth ProcessesBiologyReceptor tyrosine kinasePancreatic cancerInternal medicineCell Line TumormedicineAutophagyHumansMolecular Targeted TherapyOncogeneCell growthCancerArticlesCell cyclemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaErbB ReceptorsPancreatic Neoplasmsmedicine.anatomical_structureEndocrinologycell deathOncologyHER-2Cancer researchbiology.protein2-triazenoazaindolesTriazenesCarcinoma Pancreatic Ductal
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Effects of interferon gamma on the proliferation and modulation of cell-surface structures of human ovarian carcinoma cell lines.

1993

Platinum-containing regimens are very effective in the primary treatment of ovarian cancer. However, upon subsequent treatment most tumors develop multidrug resistance. The clinical application of biological response modifiers like interferon gamma (IFN gamma) in advanced ovarian cancer is therefore of increasing interest. Permanent ovarian cancer cell lines are suitable for investigating the mode of action and the potential clinical effectiveness of such response modifiers. IFN gamma is known to modulate many cellular functions. In this study it was compared for its antiproliferative and antigen-modulatory activity on the expression of tumor-associated (CA-125, HMFG, CEA) and major histoco…

Cancer ResearchReceptor expressionCellInterferon-gammaAntigenEpidermal growth factorAntigens NeoplasmHLA AntigensMHC class ImedicineTumor Cells CulturedHumansAntigens Tumor-Associated CarbohydrateOvarian NeoplasmsMHC class IIbiologyCell growthCell MembraneGeneral Medicinemedicine.diseaseRecombinant ProteinsErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyImmunologyAntigens Surfacebiology.proteinCancer researchFemaleOvarian cancerCell DivisionJournal of cancer research and clinical oncology
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Platelet-derived growth factor alpha mediates the proliferation of peripheral T-cell lymphoma cells via an autocrine regulatory pathway.

2014

Peripheral T-cell lymphomas not otherwise specified (PTCL/NOS) are very aggressive tumors characterized by consistent aberrant expression of platelet-derived growth factor receptor alpha (PDGFRA). In this study, we aimed to identify the determinants of PDGFRA activity in PTCL/NOS and to elucidate the biological consequences of its activation. We observed overexpression of the PDGFRA gene by gene expression profiling in most of the tested PTCLs and confirmed the expression of PDGFRA and phospho-PDGFRA using immunohistochemistry. The integrity of the PDFGRA locus was demonstrated using several different approaches, including massive parallel sequencing and Sanger sequencing. PDGF-AA was found…

Cancer ResearchReceptor Platelet-Derived Growth Factor alphamedicine.medical_treatmentT celltumor cell proliferationPDGFRAGrowth factor receptorCell Line TumormedicinePDFGRASTAT5 Transcription FactorHumansAutocrine signallingExtracellular Signal-Regulated MAP KinasesSTAT5PTCL/NOS; PDFGRA; tumor cell proliferationCell ProliferationPlatelet-Derived Growth FactorbiologyCell growthExtracellular Signal-Regulated MAP KinaseGrowth factorLymphoma T-Cell PeripheralHematologyPTCL/NOSdigestive system diseasesGene expression profilingAutocrine Communicationmedicine.anatomical_structureAnesthesiology and Pain MedicineSTAT1 Transcription FactorOncologyCancer researchbiology.proteinT-cell lymphomaProto-Oncogene Proteins c-aktHuman
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PO-053 The phospholipase ddhd1 as a new target in colorectal cancer therapy

2018

Introduction We have recently demonstrated that Citrus-limon derived nanovesicles are able to decrease colon cancer cell viability and that this effect is associated with the down-regulation of the intracellular phospholipase DDHD domain-containing protein 1 (DDHD1). While few studies are currently available on DDHD1 contribution in neurological disorders, information on its involvement in cancer is missing. Here we investigate the role of DDHD1 in colon cancer. Material and methods DDHD1 siRNAs and overexpression vector were transfected into colorectal cancer and normal cells to down-regulate or up-regulate DDHD1 expression. In vitro and in vivo assays were performed to investigate the fun…

Cancer ResearchSmall interfering RNAColorectal cancerCell growthCancerTransfectionBiologymedicine.diseaseOncologyCancer cellmedicineCancer researchGene silencingIntracellular
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