Search results for "FACTOR"

showing 10 items of 17757 documents

2018

Abstract TNFα is a prominent proinflammatory cytokine and a critical mediator for the development of many types of cancer such as breast, colon, prostate, cervical, skin, liver, and chronic lymphocytic leukemia. Binding of TNFα to TNFR1 can lead to divergent signaling pathways promoting predominantly NF-κB activation but also cell death. We report here that the nitric oxide (NO) donor glyceryl trinitrate (GTN) converts TNFα, generated from immune cells or cancer cells stimulated by chemotherapy, into a prodeath mediator in colon and mammary cancer cells. GTN-mediated S-nitrosylation of cIAP1 on cysteines 571 and 574 inhibited its E3 ubiquitin ligase activity, which in turn reduced Lys63-lin…

0301 basic medicineCancer ResearchProgrammed cell deathbiologybusiness.industryCancerInflammationmedicine.diseaseUbiquitin ligaseProinflammatory cytokine03 medical and health sciences030104 developmental biologyImmune systemOncologyCancer cellbiology.proteinCancer researchmedicineTumor necrosis factor alphamedicine.symptombusinessCancer Research
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Molecular Engineering Strategies Tailoring the Apoptotic Response to a MET Therapeutic Antibody

2020

The MET oncogene encodes a tyrosine kinase receptor involved in the control of a complex network of biological responses that include protection from apoptosis and stimulation of cell growth during embryogenesis, tissue regeneration, and cancer progression. We previously developed an antagonist antibody (DN30) inducing the physical removal of the receptor from the cell surface and resulting in suppression of the biological responses to MET. In its bivalent form, the antibody displayed a residual agonist activity, due to dimerization of the lingering receptors, and partial activation of the downstream signaling cascade. The balance between the two opposing activities is variable in different…

0301 basic medicineCancer ResearchProgrammed cell deathlcsh:RC254-282ArticleReceptor tyrosine kinase03 medical and health sciences0302 clinical medicineMET oncogenemedicineantibodiesAntibodies; Apoptosis; MET oncogene; MET targeted therapyReceptorbiologyCell growthChemistryapoptosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmet targeted therapyCell biology030104 developmental biologyOncology<i>met</i> oncogeneApoptosis030220 oncology & carcinogenesisCancer cellbiology.proteinHepatocyte growth factorAntibodymedicine.drugCancers
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Yeast Cth2 protein represses the translation of ARE-containing mRNAs in response to iron deficiency

2018

In response to iron deficiency, the budding yeast Saccharomyces cerevisiae undergoes a metabolic remodeling in order to optimize iron utilization. The tandem zinc finger (TZF)-containing protein Cth2 plays a critical role in this adaptation by binding and promoting the degradation of multiple mRNAs that contain AU-rich elements (AREs). Here, we demonstrate that Cth2 also functions as a translational repressor of its target mRNAs. By complementary approaches, we demonstrate that Cth2 protein inhibits the translation of SDH4, which encodes a subunit of succinate dehydrogenase, and CTH2 mRNAs in response to iron depletion. Both the AREs within SDH4 and CTH2 transcripts, and the Cth2 TZF are es…

0301 basic medicineCancer ResearchRNA StabilityAdaptation BiologicalGene ExpressionBiochemistryGene Expression Regulation FungalGene expressionMedicine and Health SciencesExpressió genèticaGenetics (clinical)Regulation of gene expressionZinc fingerbiologyMessenger RNANutritional DeficienciesEukaryotaTranslation (biology)Iron DeficienciesCell biologyNucleic acidsDNA-Binding ProteinsCellular Structures and OrganellesResearch ArticleSaccharomyces cerevisiae Proteinslcsh:QH426-470IronProtein subunitSaccharomyces cerevisiaeSaccharomyces cerevisiaeDNA constructionRegulatory Sequences Ribonucleic Acid03 medical and health sciencesExtraction techniquesTristetraprolinPolysomeGeneticsRNA MessengerMolecular BiologyEcology Evolution Behavior and SystematicsNutritionAU Rich ElementsAU-rich elementBiology and life sciencesOrganismsFungiCell Biologybiology.organism_classificationYeastRNA extractionResearch and analysis methodslcsh:GeneticsMolecular biology techniques030104 developmental biologyPolyribosomesPlasmid ConstructionIron DeficiencyRNAProtein TranslationRibosomesTranscription Factors
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Tumor-Associated Fibroblasts Promote HER2-Targeted Therapy Resistance through FGFR2 Activation

2020

AbstractPurpose:Despite the therapeutic success of existing HER2-targeted therapies, tumors invariably relapse. This study aimed at identifying new mechanisms responsible for HER2-targeted therapy resistance.Experimental Design:We have used a platform of HER2-targeted therapy–resistant cell lines and primary cultures of healthy and tumor-associated fibroblasts (TAF) to identify new potential targets related to tumor escape from anti-HER2 therapies.Results:We have shown that TAFs promote resistance to HER2-targeted therapies. TAFs produce and secrete high levels of FGF5, which induces FGFR2 activation in the surrounding breast cancer cells. FGFR2 transactivates HER2 via c-Src, leading to res…

0301 basic medicineCancer ResearchReceptor ErbB-2medicine.medical_treatmentMice NudeBreast NeoplasmsDrug resistanceTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerCancer-Associated FibroblastsTrastuzumabCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsmedicineNeoplasmAnimalsHumansReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesneoplasmsbusiness.industryLapatinibTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysSurvival Rate030104 developmental biologyOncologyTumor EscapeApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemaleSignal transductionNeoplasm Recurrence Localbusinessmedicine.drugSignal Transduction
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Nut1/Hos1 and Sas2/Rpd3 control the H3 acetylation of two different sets of osmotic stress-induced genes

2019

Epigenetic information is able to interact with the cellular environment and could be especially useful for reprograming gene expression in response to a physiological perturbation. In fact the genes induced or repressed by osmotic stress undergo significant changes in terms of the levels of various histone modifications, especially in the acetylation levels of histone H3. Exposing yeast to high osmolarity results in the activation of stress-activated protein kinase Hog1, which plays a central role in gene expression control. We evaluated the connection between the presence of Hog1 and changes in histone H3 acetylation in stress-regulated genes. We found a parallel increase in the acetylati…

0301 basic medicineCancer ResearchSaccharomyces cerevisiae Proteinschip-on-chipSaccharomyces cerevisiaeEpigenesis GeneticHistones03 medical and health sciencesHistone H30302 clinical medicineOsmotic PressureGene Expression Regulation FungalGene expressionEpigeneticsHistone H3 acetylationMolecular BiologyHistone AcetyltransferasesRegulation of gene expressionMediator ComplexbiologyepigeneticsAcetylationCell biologyChromatinDNA-Binding ProteinsHistone Code030104 developmental biologyHistoneHistone acetylationAcetylation030220 oncology & carcinogenesisbiology.proteinchromatinhog1osmotic stressMitogen-Activated Protein Kinasesgene regulationProtein Processing Post-TranslationalTranscription FactorsResearch Paper
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HGF/MET Axis Induces Tumor Secretion of Tenascin-C and Promotes Stromal Rewiring in Pancreatic Cancer

2021

Simple Summary It has been previously shown that activation of the MET receptor by its ligand, the hepatocyte growth factor (HGF), modulates the tumor-stroma cross-talk in models of pancreatic cancer. We now wish to cast light on the molecular mechanisms by which this ligand/receptor pair sustains the interaction between cancer cells and the tumor microenviroment. To this end, we compared data obtained by large-scale analysis of gene expression in pancreatic cancer cells grown in the presence of HGF versus cells grown in the presence of HGF and treated with specific inhibitors of HGF/MET signaling. By clustering differentially expressed genes according to functional groups, we identified ca…

0301 basic medicineCancer ResearchStromal cellpancreatic ductal adenocarcinomaArticle03 medical and health sciences0302 clinical medicinePancreatic tumorPancreatic cancerMET oncogenemedicinetumor microenvironmentmetastasisHepatocyte growth factor; MET oncogene; Metastasis; Pancreatic ductal adenocarcinoma; Tenascin C; Tumor microenvironmentRC254-282Tumor microenvironmentbiologyChemistryTenascin Ctenascin CNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyhepatocyte growth factorOncology030220 oncology & carcinogenesisCancer cellHepatic stellate cellbiology.proteinCancer researchHepatocyte growth factormedicine.drugCancers
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Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

2017

Abstract Thyroid carcinoma is generally associated with good prognosis, but no effective treatments are currently available for aggressive forms not cured by standard therapy. To find novel therapeutic targets for this tumor type, we had previously performed a siRNA-based functional screening to identify genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same extent for the viability of normal cells (non-oncogene addiction paradigm). Among those, we found the coatomer protein complex ζ1 (COPZ1) gene, which is involved in intracellular traffic, autophagy and lipid homeostasis. In this paper, we investigated the mechanisms through which COPZ…

0301 basic medicineCancer ResearchTime FactorsCOPZ1ApoptosisCOPZ1Thyroid cancerThyroid NeoplasmThyroidRNAi TherapeuticCell death; COPZ1; Non-oncogene addiction; Thyroid carcinoma; Animals; Apoptosis; Autophagy; Cell Line Tumor; Cell Survival; Coatomer Protein; Endoplasmic Reticulum Stress; Female; Gene Expression Regulation Neoplastic; Humans; Mice Nude; RNA Interference; Signal Transduction; Thyroid Neoplasms; Time Factors; Transfection; Tumor Burden; Unfolded Protein Response; Xenograft Model Antitumor Assays; RNAi Therapeutics; Oncology; Cancer ResearchEndoplasmic Reticulum StressOncogene AddictionTumor BurdenGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyFemaleRNA InterferenceNon-oncogene addictionHumanSignal TransductionCell deathProgrammed cell deathXenograft Model Antitumor AssayTime FactorCell SurvivalMice NudeBiologyTransfectionCoatomer ProteinThyroid carcinomaThyroid carcinoma03 medical and health sciencesCell Line TumorAutophagymedicineAnimalsHumansThyroid NeoplasmsEndoplasmic Reticulum StreAnimalAutophagyApoptosimedicine.diseaseXenograft Model Antitumor AssaysRNAi Therapeutics030104 developmental biologyImmunologyUnfolded Protein ResponseCancer researchUnfolded protein response
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Chronic Sulforaphane Application Does Not Induce Resistance in Renal Cell Carcinoma Cells.

2018

Background/aim Since the natural compound sulforaphane (SFN) has been shown to stop tumor growth, renal cell carcinoma (RCC) patients often use this drug in addition to their prescribed oncotherapy. The aim of this study was to examine whether resistance to SFN may develop after long-term application. Materials and methods Several RCC cell lines were incubated with SFN for short periods of time (24-72 h) or long periods of time (8 weeks) and cell growth, proliferation, and cell-cycle proteins were analyzed. Results Both short- and long-term application of SFN distinctly reduced RCC cell growth and proliferation. However, differences in the distribution of cells in each phase of the cell cyc…

0301 basic medicineCancer ResearchTime FactorsCell SurvivalCell Cycle Proteins03 medical and health scienceschemistry.chemical_compoundIsothiocyanatesCell Line TumorAnticarcinogenic AgentsHumansPhosphorylationProtein kinase BCarcinoma Renal CellCell ProliferationCyclin-dependent kinase 1biologyCell growthCyclin-dependent kinase 2General MedicineCell cycleKidney NeoplasmsGene Expression Regulation Neoplastic030104 developmental biologyOncologychemistryCell cultureA549 CellsDrug Resistance NeoplasmSulfoxidesCancer researchbiology.proteinSignal transductionDrug Screening Assays AntitumorSulforaphaneSignal TransductionAnticancer research
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Inhibition of colon cancer growth by docosahexaenoic acid involves autocrine production of TNFα

2016

IF 7.932; International audience; The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) has anti-inflammatory and anti-cancer properties. Among pro-inflammatory mediators, tumor necrosis factor a (TNF alpha) plays a paradoxical role in cancer biology with induction of cancer cell death or survival depending on the cellular context. The objective of the study was to evaluate the role of TNFa in DHA-mediated tumor growth inhibition and colon cancer cell death. The treatment of human colorectal cancer cells, HCT-116 and HCT-8 cells, with DHA triggered apoptosis in autocrine TNF alpha-dependent manner. We demonstrated that DHA-induced increased content of TNF alpha mRNA occurred thr…

0301 basic medicineCancer ResearchTumoricidal ActionApoptosis[ SDV.CAN ] Life Sciences [q-bio]/CancerMice[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsForkhead Box Protein O3Cell cycle3. Good healthCell biologyGene Expression Regulation NeoplasticAutocrine CommunicationColonic NeoplasmsTumor-Necrosis-FactorTumor necrosis factor alphaProgrammed cell deathDocosahexaenoic AcidsHuman Colorectal-CancerGene-Expression[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesGrowth factor receptorLipid-MetabolismGeneticsmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCell-DeathPolyunsaturated Fatty-AcidsAutocrine signallingMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyActivated Protein-KinaseTumor Necrosis Factor-alpha[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyInduced ApoptosisCancerHCT116 Cellsmedicine.diseaseXenograft Model Antitumor AssaysMicroRNAs030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsApoptosisCancer cellCancer researchPrevents Breast-Cancer
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Editorial: Cell Stress, Metabolic Reprogramming, and Cancer

2018

0301 basic medicineCancer Researchantioxidant responseAntioxidant response; Ataxia-telangiectasia mutated; Cancer; Epithelial-to-mesenchymal transition; Glutamine; Hypoxia-inducible factor 1 alpha; L-lactate; Mitochondria; Oncology; Cancer ResearchMetabolic reprogrammingMitochondrionBiologylcsh:RC254-28203 medical and health sciencesHypoxia-Inducible Factor 1-AlphamedicinecancerGlycolysisEpithelial–mesenchymal transitionataxia-telangiectasia mutatedCancerL-lactatemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensGlutaminemitochondriaCell stress030104 developmental biologyEditorialOncologyCancer researchglutaminehypoxia-inducible factor 1 alphaepithelial-to-mesenchymal transition
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