Search results for "Oncogene"

showing 10 items of 1005 documents

Analysis of the expression of SDF-1 splicing variants in human colorectal cancer and normal mucosa tissues

2016

C-X-C motif chemokine ligand 12 (CXCL12), also termed stromal cell-derived factor-1 (SDF-1) is a small protein 8-14 kDa in length that is expressed as six isoforms, consisting of SDF-1α, SDF-1β, SDF-1γ, SDF-1δ, SDF-1ε and SDF-1θ. All six isoforms are encoded by the single CXCL12 gene on chromosome 10. This gene regulates leukocyte trafficking and is variably expressed in a number of normal and cancer tissues. The potential role of the novel CXCL12 splice variants as components of the CXCR4 axis in cancer development is not fully understood. The present study aimed to analyze the expression profile of the various SDF-1 isoforms and SDF-1 polymorphisms, and the association with the clinicopat…

0301 basic medicineGene isoformCancer ResearchPathologymedicine.medical_specialtyOncogeneArticlesBiologymedicine.diseasePrimary tumorCXCR403 medical and health sciences030104 developmental biology0302 clinical medicineOncologyTumor progression030220 oncology & carcinogenesisGenotypemedicineCancer researchGene polymorphismTumor markerOncology Letters
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ΔNp63 drives metastasis in breast cancer cells via PI3K/CD44v6 axis

2016

P63 is a transcription factor belonging to the family of p53, essential for the development and differentiation of epithelia. In recent years, it has become clear that altered expression of the different isoforms of this gene can play an important role in carcinogenesis. The p63 gene encodes for two main isoforms known as TA and ΔN p63 with different functions. The role of these different isoforms in sustaining tumor progression and metastatic spreading however has not entirely been clarified. Here we show that breast cancer initiating cells express ΔNp63 isoform that supports a more mesenchymal phenotype associated with a higher tumorigenic and metastatic potential. On the contrary, the ma…

0301 basic medicineGene isoformEpithelial-Mesenchymal TransitionBreast Neoplasmsmedicine.disease_causeMetastasisMicePhosphatidylinositol 3-Kinases03 medical and health sciencesBreast cancerTumor MicroenvironmentmedicineAnimalsHumansmetastasisEpithelial–mesenchymal transitionNeoplasm MetastasisPI3K/AKT/mTOR pathwayAgedAged 80 and overTumor microenvironmentp63breast cancer initiating cellsbusiness.industryMembrane ProteinsCD44v6Middle Agedmedicine.diseasePI3K/AKT pathwayHyaluronan Receptors030104 developmental biologyOncologyDrug Resistance NeoplasmTumor progressionImmunologyCancer researchFemalebreast cancer initiating cellmetastasibusinessCarcinogenesisProto-Oncogene Proteins c-aktSignal TransductionPriority Research Paper
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The MDS and EVI1 complex locus (MECOM) isoforms regulate their own transcription and have different roles in the transformation of hematopoietic stem…

2016

Transcriptional activation of the EVI1 oncogene (3q26) leads to aggressive forms of human acute myeloid leukemia (AML). However, the mechanism of EVI1-mediated leukemogenesis has not been fully elucidated. Previously, by characterizing the EVI1 promoter, we have shown that RUNX1 and ELK1 directly regulate EVI1 transcription. Intriguingly, bioinformatic analysis of the EVI1 promoter region identified the presence of several EVI1 potential binding sites. Thus, we hypothesized that EVI1 could bind to these sites regulating its own transcription. In this study, we show that there is a functional interaction between EVI1 and its promoter, and that the different EVI1 isoforms (EVI1-145kDa, EVI1-Δ…

0301 basic medicineGene isoformMECOMResponse elementBiophysicsBiologyBiochemistryCell LineMice03 medical and health scienceschemistry.chemical_compoundStructural BiologyTranscription (biology)Proto-OncogenesGeneticsAnimalsHumansProgenitor cellPromoter Regions GeneticMolecular BiologyTranscription factorGeneticsLeukemiaGene Expression Regulation LeukemicPromoterHematopoietic Stem CellsMDS1 and EVI1 Complex Locus ProteinCell biologyDNA-Binding ProteinsCell Transformation Neoplastic030104 developmental biologyRUNX1chemistryTranscription FactorsBiochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms
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DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas.

2018

Granulomas are immune cell aggregates formed in response to persistent inflammatory stimuli. Granuloma macrophage subsets are diverse and carry varying copy numbers of their genomic information. The molecular programs that control the differentiation of such macrophage populations in response to a chronic stimulus, though critical for disease outcome, have not been defined. Here, we delineate a macrophage differentiation pathway by which a persistent Toll-like receptor (TLR) 2 signal instructs polyploid macrophage fate by inducing replication stress and activating the DNA damage response. Polyploid granuloma-resident macrophages formed via modified cell divisions and mitotic defects and not…

0301 basic medicineGenome instabilityDNA damageLipoproteinsCellMitosisInflammationAtaxia Telangiectasia Mutated ProteinsBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicemedicineAnimalsHumansMacrophage Differentiation PathwayMitosisCell ProliferationInflammationGranulomaMacrophagesCell DifferentiationMycobacterium tuberculosisToll-Like Receptor 2Cell biologyMice Inbred C57BLTLR2030104 developmental biologymedicine.anatomical_structureImmunologymedicine.symptomCarcinogenesisDNA DamageCell
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Functional inhibition of Oct leads to HNF4α upregulation

2021

Organic cation transporters (human, OCT; mouse, Oct) are responsible for the intracellular uptake and detoxification of a broad spectrum of endogenous and exogenous substrates. The OCT1 gene SLC22A1 (human; mouse, Scl22a1) is transactivated by hepatocyte nuclear factor 4α (human, HNF4α; mouse, Hnf4α). HNF4α is a master regulator of hepatocyte differentiation and is frequently associated with hepatocellular carcinoma (HCC). In addition, the downregulation of HNF4α is associated with enhanced fibrogenesis. Our recent study revealed that hepatocarcinogenesis and fibrosis were enhanced with the loss of Oct3 (gene, Slc22a3). Notably, differences in Hnf4α expression, and in cholestasis and fibros…

0301 basic medicineHepatocyte differentiationCancer ResearchOncogeneChemistryArticlesGeneral Medicineorganic cation transportermedicine.diseaseMolecular biology03 medical and health sciencesHepatocyte nuclear factors030104 developmental biology0302 clinical medicineImmunology and Microbiology (miscellaneous)CholestasisDownregulation and upregulationApoptosisFibrosis030220 oncology & carcinogenesisGene expressionmedicineSLC22A3HNF4αSLC22A1Experimental and Therapeutic Medicine
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Frontline Science: Mast cells regulate neutrophil homeostasis by influencing macrophage clearance activity

2019

Abstract The receptor tyrosine kinase cKit and its ligand stem cell factor are essential for mast cells (MC) development and survival. Strains with mutations affecting the Kit gene display a profound MC deficiency in all tissues and have been extensively used to investigate the role of MC in both physiologic and pathologic conditions. However, these mice present a variety of abnormalities in other immune cell populations that can affect the interpretation of MC-related responses. C57BL/6 KitW-sh are characterized by an aberrant extramedullary myelopoiesis and systemic neutrophilia. MC deficiency in KitW-sh mice can be selectively repaired by engraftment with in vitro-differentiated MC to va…

0301 basic medicineImmunologyKit (W-sh) mice; macrophages; mast cell; neutrophils; phagocytosisBone Marrow CellsCell CountStem cell factormacrophageReceptor tyrosine kinase03 medical and health sciences0302 clinical medicineImmune systemneutrophilsGranulocyte Colony-Stimulating FactormedicineAnimalsHomeostasisImmunology and AllergyMacrophageMyeloid CellsMast CellsNeutrophil homeostasisCD11b AntigenNeutrophil clearancebiologyInterleukin-17neutrophilphagocytosisCell BiologyKit (W-sh) miceNeutrophiliaHematopoiesismacrophagesCell biologyMice Inbred C57BLProto-Oncogene Proteins c-kitPhenotype030104 developmental biologybiology.proteinCytokinesInflammation Mediatorsmedicine.symptommast cellEx vivoSignal Transduction030215 immunologyJournal of Leukocyte Biology
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The Cytoskeletal Adaptor Obscurin-Like 1 Interacts with the Human Papillomavirus 16 (HPV16) Capsid Protein L2 and Is Required for HPV16 Endocytosis.

2016

ABSTRACT The human papillomavirus (HPV) capsid protein L2 is essential for viral entry. To gain a deeper understanding of the role of L2, we searched for novel cellular L2-interacting proteins. A yeast two-hybrid analysis uncovered the actin-depolymerizing factor gelsolin, the membrane glycoprotein dysadherin, the centrosomal protein 68 (Cep68), and the cytoskeletal adaptor protein obscurin-like 1 protein (OBSL1) as putative L2 binding molecules. Pseudovirus (PsV) infection assays identified OBSL1 as a host factor required for gene transduction by three oncogenic human papillomavirus types, HPV16, HPV18, and HPV31. In addition, we detected OBSL1 expression in cervical tissue sections and no…

0301 basic medicineKeratinocytesvirusesImmunologyEndocytic cycleEndocytosisMicrobiologyClathrinCell Line03 medical and health sciencesTransduction (genetics)TetraspaninViral entryVirologyTwo-Hybrid System TechniquesCaveolinHumansHuman papillomavirus 16biologyPapillomavirus InfectionsSignal transducing adaptor proteinOncogene Proteins ViralVirus InternalizationEndocytosisCell biologyVirus-Cell InteractionsCytoskeletal Proteins030104 developmental biologyInsect ScienceGene Knockdown TechniquesHost-Pathogen Interactionsbiology.proteinCapsid ProteinsHeLa CellsJournal of virology
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Anticancer potential of novel α,β-unsaturated γ-lactam derivatives targeting the PI3K/AKT signaling pathway.

2021

Abstract Six recently synthesized alkyl (Z)-2-(2-oxopyrrolidin-3-ylidene)acetates were evaluated for their potential as cytotoxic and anticancer agents. All compounds were tested in the ERα positive MCF-7, triple negative MDA-MB-231, and Her2+ SKBR-3 breast cancer cell lines. The most lipophilic derivatives, bearing the 4-isopropylphenyl (2) or 4-tert-butylphenyl (3) group at the γ-lactam nitrogen, proved to be cytotoxic against all the cancer cell lines tested (IC50 values ranging from 18 to 63 μM), exerting their greatest activity in SKBR-3 cells, with IC50 values of 33 and 18 μM, respectively. Biological studies showed that the cytotoxic effects of 2 and 3 are accompanied by apoptotic de…

0301 basic medicineLactamsCell SurvivalAntineoplastic AgentsApoptosisBreast NeoplasmsBiochemistry03 medical and health scienceschemistry.chemical_compoundPI3K/AKT signaling pathwayPhosphatidylinositol 3-Kinases0302 clinical medicinebreast cancerCytotoxic T cellHumansα-methylene-γ-lactamsαβ-unsaturated lactamsCytotoxicityPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsPharmacologychemistry.chemical_classificationBiological ProductsMolecular StructureChemistryCell growthAkt/PKB signaling pathwayCell CycleEpithelial Cells030104 developmental biologyEnzymeGene Expression RegulationApoptosis030220 oncology & carcinogenesisCancer researchLactamcytotoxicityFemaleProto-Oncogene Proteins c-aktBiochemical pharmacology
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Nuclear Translocation of RELB Is Increased in Diseased Human Liver and Promotes Ductular Reaction and Biliary Fibrosis in Mice.

2019

Background & Aims Cholangiocyte proliferation and ductular reaction contribute to the onset and progression of liver diseases. Little is known about the role of the transcription factor nuclear factor-κB (NF-κB) in this process. We investigated the activities of the RELB proto-oncogene NF-κB subunit in human cholangiocytes and in mouse models of liver disease characterized by a ductular reaction. Methods We obtained liver tissue samples from patients with primary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or C virus infection, autoimmune hepatitis, alcoholic liver disease, or without these diseases (controls) from a tissue bank in Germany. Tissues were analyzed by immu…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCholangiocyte proliferationAutoimmune hepatitisProto-Oncogene MasLiver diseaseMice0302 clinical medicineCarbon TetrachlorideCells CulturedRELBLiver DiseasesGastroenterologyMiddle Aged3. Good healthDeubiquitinating Enzyme CYLDCysteine EndopeptidasesProtein TransportLiverGene Knockdown TechniquesCytokines030211 gastroenterology & hepatologyFemaleCell activationAdultLymphotoxin-betaAdolescentCholangitis SclerosingPrimary sclerosing cholangitis03 medical and health sciencesYoung AdultLymphotoxin beta ReceptormedicineAnimalsHumansRNA MessengerParenchymal TissueAgedCell ProliferationCell NucleusHepatologybusiness.industryTranscription Factor RelBEpithelial CellsDicarbethoxydihydrocollidinemedicine.diseaseFibrosis030104 developmental biologyCancer researchLiver functionBile DuctsbusinessGastroenterology
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MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibition

2017

Advanced lung cancer has poor survival with few therapies. EGFR tyrosine kinase inhibitors (TKIs) have high response rates in patients with activating EGFR mutations, but acquired resistance is inevitable. Acquisition of the EGFR T790M mutation causes over 50% of resistance; MET amplification is also common. Preclinical data suggest synergy between MET and EGFR inhibitors. We hypothesized that EGFR-MET dimerization determines response to MET inhibition, depending on EGFR mutation status, independently of MET copy number. We tested this hypothesis by generating isogenic cell lines from NCI-H1975 cells, which co-express L858R and T790M EGFR mutations, namely H1975L858R/T790M (EGFR TKI resista…

0301 basic medicineLung NeoplasmsKinase InhibitorsCancer Treatmentlcsh:MedicinePhysical ChemistryBiochemistryFluorophotometryT790MSpectrum Analysis Techniques0302 clinical medicineFluorescence Resonance Energy TransferMedicine and Health SciencesPhosphorylationEnzyme Inhibitorslcsh:ScienceExtracellular Signal-Regulated MAP KinasesEGFR inhibitorsStainingMice Inbred BALB CMultidisciplinaryFluorescent in Situ HybridizationPhysicsCell StainingProto-Oncogene Proteins c-metPrecipitation TechniquesErbB ReceptorsChemistryOncologySpectrophotometry030220 oncology & carcinogenesisPhysical SciencesErlotinibDimerizationProtein BindingResearch Articlemedicine.drugChemical physicsMice NudeMolecular Probe TechniquesAdenocarcinoma of LungAdenocarcinomaBiologyResearch and Analysis Methods03 medical and health sciencesGefitinibGrowth factor receptorCell Line TumormedicineAnimalsHumansImmunoprecipitationMolecular Biology TechniquesLung cancerProtein Kinase InhibitorsMolecular BiologyCell ProliferationCell growthlcsh:RReproducibility of ResultsBiology and Life SciencesDimers (Chemical physics)medicine.diseaseMolecular biologyIsogenic human disease modelsProbe Hybridizationrespiratory tract diseasesHEK293 Cells030104 developmental biologyChemical PropertiesSpecimen Preparation and TreatmentFocal Adhesion Protein-Tyrosine KinasesMutationEnzymologylcsh:QProtein MultimerizationProto-Oncogene Proteins c-aktCytogenetic TechniquesPLOS ONE
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