Search results for "Bcl-2"

showing 10 items of 197 documents

Expression of Bax, a pro-apoptotic member of the Bcl-2 family, in esophageal squamous cell carcinoma

1997

Samples of normal esophageal squamous epithelium (n = 10), severe squamous cell dyplasia (n = 22), carcinoma in situ (n = 15), invasive squamous cell carcinoma (n = 172), lymph-node metastasis (n = 21) and 2 permanent esophageal squamous cell carcinoma cell lines were analyzed immunohistochemically for Bax expression using a polyclonal anti-Bax antibody. Immunostaining was evaluated according to a score system (0–8 points) based on the percentage of positive tumor cells and the relative immunostaining intensity. Cytoplasmatic staining for Bax protein was found uniformly in all cell layers of the normal esophageal squamous epithelium. In contrast, a gradual loss of immunoreactivity for Bax w…

AdultMaleCancer ResearchPathologymedicine.medical_specialtyEsophageal NeoplasmsCellBiologyMetastasisEsophagusProto-Oncogene ProteinsTumor Cells CulturedmedicineHumansEsophagusAgedbcl-2-Associated X ProteinAged 80 and overCarcinoma in situCancerMiddle AgedEsophageal cancermedicine.diseaseSurvival AnalysisNeoplasm Proteinsmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyEpidermoid carcinomaCarcinoma Squamous CellRegression AnalysisFemaleCarcinoma in SituImmunostainingInternational Journal of Cancer
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bcl-2 expression and prognosis in squamous-cell carcinomas of the esophagus

1996

The bcl-2 proto-oncogene is a known inhibitor of apoptosis and may be an important regulator of tumor growth. In the present study, bcl-2-protein expression was investigated by immunohistochemistry and correlated with prognosis in a series of 150 potentially curatively resected squamous-cell carcinomas of the esophagus. For comparison, bcl-2-protein expression was analyzed in normal esophageal mucosa, severe squamous dysplasias and carcinomas in situ. bcl-2 immunoreactivity was found in 40 out of 150 invasive squamous-cell carcinomas; the remaining carcinomas were completely negative. bcl-2-protein expression was found more frequently among poorly differentiated than among well-differentiat…

AdultCancer ResearchPathologymedicine.medical_specialtyEsophageal NeoplasmsCellGene ExpressionBiologyInhibitor of apoptosisProto-Oncogene MasProto-Oncogene ProteinsGene expressionmedicineHumansEsophagusAgedAged 80 and overMucous MembraneEsophageal diseaseMiddle AgedEsophageal cancerPrognosismedicine.diseaseSurvival Ratemedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyEpidermoid carcinomaCarcinoma Squamous CellImmunohistochemistryCarcinoma in SituInternational Journal of Cancer
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Down-regulation of Glutathione and Bcl-2 Synthesis in Mouse B16 Melanoma Cells Avoids Their Survival during Interaction with the Vascular Endothelium

2003

B16 melanoma (B16M) cells with high GSH content show high metastatic activity. However, the molecular mechanisms linking GSH to metastatic cell survival are unclear. The possible relationship between GSH and the ability of Bcl-2 to prevent cell death was studied in B16M cells with high (F10) and low (F1) metastatic potential. Analysis of a Bcl-2 family of genes revealed that B16M-F10 cells, as compared with B16M-F1 cells, overexpressed preferentially Bcl-2 (approximately 5.7-fold). Hepatic sinusoidal endothelium-induced B16M-F10 cytotoxicity in vitro increased from approximately 19% (controls) to approximately 97% in GSH-depleted B16M-F10 cells treated with an antisense Bcl-2 oligodeoxynucl…

MaleProgrammed cell deathPore complexCell SurvivalMelanoma ExperimentalDown-RegulationOxidative phosphorylationBiologyBiochemistryOligodeoxyribonucleotides AntisenseMicechemistry.chemical_compoundDownregulation and upregulationCell Line TumorAnimalsButhionine SulfoximineMolecular BiologyBase SequenceTransition (genetics)Cell BiologyGlutathioneGlutathioneMolecular biologyGenes bcl-2Cell biologyMice Inbred C57BLOxidative StressCytosolchemistryEndothelium VascularEffluxCell DivisionJournal of Biological Chemistry
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The effect of 3-aminobenzamide, inhibitor of poly(ADP-ribose) polymerase, on human osteosarcoma cells

2003

This study demonstrates that in human osteosarcoma cells treatment with 3-aminobenzamide (3-AB), a potent inhibitor of poly(ADP-ribose) polymerase (PARP), induces morphological and biochemical features of differentiation, the duration of which depends on whether or not the normal RB gene is expressed. In Saos-2 cells expressing a non-functional Rb protein, 3-AB treatment induced the formation of transient, short dendritic-like protrusions. In RB-transfected-Saos-2 cells (a clone previously generated in our laboratory that shows stable expression of wild-type Rb protein), 3-AB induced marked and prolonged changes with the formation of long dendritic-like protrusions and the appearance of ste…

Cancer ResearchProgrammed cell deathCell typeTime FactorsTranscription GeneticCell SurvivalPoly ADP ribose polymeraseCellular differentiationBlotting WesternApoptosisDNA FragmentationPoly(ADP-ribose) Polymerase InhibitorsBiologyTransfectionPolymerase Chain ReactionRetinoblastoma Proteinchemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsHumansMicroscopy Phase-ContrastRNA MessengerEnzyme Inhibitorsbcl-2-Associated X ProteinOsteosarcomaLamin Type BCaspase 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationDendritesCell cycleAlkaline PhosphataseFlow CytometryMolecular biologyChromatinHyaluronan ReceptorsProto-Oncogene Proteins c-bcl-2OncologychemistryApoptosis3-AminobenzamideCaspasesBenzamides3-aminobenzamide osteosarcoma cells PARP activityAlkaline phosphataseInternational Journal of Oncology
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Retinoic Acid Induces Apoptosis-Associated Neural Differentiation of a Murine Teratocarcinoma Cell Line

2002

Abstract: Incubation with all-trans retinoic acid (RA) induces PCC7-Mz1 embryonic carcinoma cells to cease proliferation and to develop into a tissue-like pattern of neuronal, astroglial, and fibroblast-like derivatives over a period of several days. Concomitant with the induction of differentiation by RA, a sizable fraction of the Mz1 stem cells detaches and dies, with the maximal level of cell death achieved after 10 h of RA treatment. This RA-induced cell death fulfills all criteria of apoptosis, including nuclear condensation, intranucleosomal DNA degradation, expression of cysteine aspases (caspases), and the formation of apoptotic bodies. Apoptosis could be suppressed by the pan-caspa…

TeratocarcinomaProgrammed cell deathCellular differentiationRetinoic acidApoptosisTretinoinBiochemistryMiceCellular and Molecular Neurosciencechemistry.chemical_compoundGAP-43 ProteinTumor Cells CulturedAnimalsProtein Kinase CProtein kinase CCaspaseNeuronsbiologyCell DifferentiationGenes bcl-2Cell biologyGene Expression RegulationchemistryBiochemistryCell cultureApoptosisPhorbolbiology.proteinJournal of Neurochemistry
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Identification of biphenyl-based hybrid molecules able to decrease the intracellular level of Bcl-2 protein in Bcl-2 overexpressing leukemia cells.

2009

Leukemia cellBCL-2Terphenyls
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Melatonin induces transcriptional regulation of Bim by FoxO3a in HepG2 cells

2012

Background: Melatonin induces apoptosis in many different cancer cell lines, including hepatocellular carcinoma cells. However, the responsible pathways have not been clearly elucidated. A member of the forkhead transcription factors' family, FoxO3a, has been implicated in the expression of the proapoptotic protein Bim (a Bcl-2-interacting mediator of cell death). In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate whether melatonin treatment induces Bim through regulation by the transcription factor FoxO3a. Methods: Cytotoxicity of melatonin was compared in HepG2 hepatoblastoma cells and primary human hepatocytes. Proapoptotic Bim expression was analys…

Transcriptional ActivationCancer Researchmedicine.medical_specialtyProgrammed cell deathSmall interfering RNACarcinoma HepatocellularTranscription GeneticApoptosisFoxO3amelatoninBiologyGenetics & GenomicsMelatoninDownregulation and upregulationCell Line TumorProto-Oncogene ProteinsInternal medicinemedicineTranscriptional regulationHumansGene silencingBimPhosphorylationRNA Small InterferingPromoter Regions GeneticTranscription factorBinding SitesBcl-2-Like Protein 11Forkhead Box Protein O3Membrane ProteinsForkhead Transcription FactorsHep G2 Cellshepatocellular carcinomaCell biologyEndocrinologyOncologyHepatocytesRNA Interferencebiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsChromatin immunoprecipitationProtein Bindingmedicine.drugBritish Journal of Cancer
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Study of Proliferation and Apoptosis in Neuroblastoma. Their Relation with Other Prognostic Factors

2002

Abstract Background Our objective was to study the proliferation and apoptotic process in 111 cases of neuroblastoma (NB) and to seek their relationship with other prognostic factors and survival. Methods Immunohistochemistry following ABC peroxidase was carried out for PCNA, Ki-67, bcl-2, and p53 proteins. Apoptosis analysis was performed with in situ detection of chromosomal breakdown. Molecular detection of DNA ladders by electrophoresis and amplification of MYCN was studied with PCR and Southern blot. Statistical study was performed with Pearson χ 2 and Kruskal-Wallis tests and Cox regression. Results Our results indicate that proliferative factors PCNA and Ki-67 were correlated to each…

MaleIn situProgrammed cell deathTime FactorsMitosisApoptosisPolymerase Chain ReactionNeuroblastomachemistry.chemical_compoundProliferating Cell Nuclear AntigenNeuroblastomamedicineHumansChildSouthern blotbiologyInfant NewbornInfantCell DifferentiationDNAGeneral MedicinePrognosismedicine.diseaseImmunohistochemistryMolecular biologyProliferating cell nuclear antigenBlotting SouthernKi-67 AntigenProto-Oncogene Proteins c-bcl-2chemistryApoptosisChild PreschoolMultivariate Analysisbiology.proteinImmunohistochemistryFemaleTumor Suppressor Protein p53Cell DivisionDNAFollow-Up StudiesArchives of Medical Research
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Thyroid Cancer Resistance to Chemotherapeutic Drugs via Autocrine Production of Interleukin-4 and Interleukin-10

2003

We investigated the mechanisms responsible for the widespread refractoriness to chemotherapeutic drugs observed in thyroid cancers. We show that malignant epithelial cells from papillary, follicular, and anaplastic thyroid carcinomas express high levels of Bcl-2 and Bcl-xL. Exogenous expression of either Bcl-2 or Bcl-xL in normal thyrocytes was sufficient to prevent chemotherapeutic drug-induced cytotoxicity. All of the histological thyroid cancer variants examined produced interleukin-4 (IL-4) and interleukin-10 (IL-10), which increased Bcl-2 and Bcl-xL levels and protected thyroid cells from chemotherapeutic agents. Exposure to neutralizing antibodies against IL-4 and IL-10 resulted in do…

Cancer ResearchCell DeathPaclitaxelCancer Research; OncologyCarcinomaThyroid Glandbcl-X ProteinAntineoplastic AgentsApoptosisThyroid Cancer Interleukin-4 Interleukin-10Middle AgedCarcinoma PapillaryInterleukin-10OncologyProto-Oncogene Proteins c-bcl-2Settore MED/04 - PATOLOGIA GENERALEDoxorubicinDrug Resistance NeoplasmHumansInterleukin-4Thyroid NeoplasmsCisplatinAged
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Absence of correlation between oxysterol accumulation in lipid raft microdomains, calcium increase, and apoptosis induction on 158N murine oligodendr…

2013

There is some evidence that oxidized derivatives of cholesterol, 7-ketocholesterol (7KC) and 7β-hydroxycholesterol (7βOHC), are increased in the plasma of patients with neurodegenerative diseases associated with demyelinization of the central nervous system (CNS). It was therefore of interest to investigate the effects of these oxysterols on oligodendrocytes, the myelin-forming cells in the CNS. To this end, 158N murine oligodendrocytes were treated with 7KC or 7βOHC inducing an apoptotic mode of cell death characterized by condensation/fragmentation of the nuclei, dephosphorylation of Akt and GSK3, mitochondrial depolarization involving Mcl-1, and caspase-3 activation. In contrast, under t…

Programmed cell deathOxysterolCell Survivalalpha-TocopherolApoptosisBiologyBiochemistryCell Linechemistry.chemical_compoundGlycogen Synthase Kinase 3MiceMembrane MicrodomainsAnimalsFragmentation (cell biology)Protein kinase BLipid raftKetocholesterolsCell ProliferationPharmacologyDepolarizationHydroxycholesterolsCell biologyOligodendrogliaSterolschemistryProto-Oncogene Proteins c-bcl-2ApoptosisIonomycinMyeloid Cell Leukemia Sequence 1 Proteinlipids (amino acids peptides and proteins)CalciumProto-Oncogene Proteins c-aktBiochemical pharmacology
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