Search results for "Lula"

showing 10 items of 7309 documents

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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Spanish Cell Therapy Network (TerCel): 15 years of successful collaborative translational research

2019

On behalf of TerCel

0301 basic medicineCancer ResearchResearch groupsBiomedical ResearchAllogeneic cellImmunologyCell- and Tissue-Based TherapyResearch networkTranslational researchStem cellsRegenerative MedicineCell therapyTranslational Research Biomedical03 medical and health sciences0302 clinical medicinePolitical scienceAgency (sociology)Immunology and AllergyHumansProduct (category theory)Intersectoral CollaborationGenetics (clinical)TransplantationMedical educationGovernmentBiología celularTranslational medicineNeurodegenerative DiseasesCell BiologyClinical trial030104 developmental biologyOncologyImmune System DiseasesCardiovascular DiseasesSpain030220 oncology & carcinogenesisRegenerative medicineTranslational medicine
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Parthenolide prevents resistance of MDA-MB231 cells to doxorubicin and mitoxantrone: the role of Nrf2.

2017

Triple-negative breast cancer is a group of aggressive cancers with poor prognosis owing to chemoresistance, recurrence and metastasis. New strategies are required that could reduce chemoresistance and increases the effectiveness of chemotherapy. The results presented in this paper, showing that parthenolide (PN) prevents drug resistance in MDA-MB231 cells, represent a contribution to one of these possible strategies. MDA-MB231 cells, the most studied line of TNBC cells, were submitted to selection treatment with mitoxantrone (Mitox) and doxorubicin (DOX). The presence of resistant cells was confirmed through the measurement of the resistance index. Cells submitted to this treatment exhibit…

0301 basic medicineCancer ResearchSmall interfering RNATriple-negative breast cancer resistance parthenolideImmunologyStimulationCancer -- TreatmentArticle03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineDownregulation and upregulationSettore BIO/10 - BiochimicamedicineChemotherapyDoxorubicinParthenolideBreast -- CancerDrug resistance in cancer cellsMitoxantroneChemistryCell BiologyTransfectionHsp70030104 developmental biology030220 oncology & carcinogenesisCancer researchmedicine.drugCell death discovery
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The tumour microenvironment as an integrated framework to understand cancer biology

2019

Cancer cells all share the feature of being immersed in a complex environment with altered cell-cell/cell-extracellular element communication, physicochemical information, and tissue functions. The so-called tumour microenvironment (TME) is becoming recognised as a key factor in the genesis, progression and treatment of cancer lesions. Beyond genetic mutations, the existence of a malignant microenvironment forms the basis for a new perspective in cancer biology where connections at the system level are fundamental. From this standpoint, different aspects of tumour lesions such as morphology, aggressiveness, prognosis and treatment response can be considered under an integrated vision, givin…

0301 basic medicineCancer ResearchStromal cellBiophysicsDiseaseBiologyExtracellular matrix03 medical and health sciences0302 clinical medicineGermline mutationImmune systemNeoplasmsTumor MicroenvironmentmedicineStromal classificationAnimalsHumansCompartment (development)CancerExtracellular matrixmedicine.diseaseBioelectricExtracellular MatrixMetabolism030104 developmental biologyOncologyCancer treatment030220 oncology & carcinogenesisCancer cellStromal CellsNeuroscienceCancer Letters
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Cancer-associated fibroblasts as abettors of tumor progression at the crossroads of EMT and therapy resistance

2019

Abstract In the last decades, the role of the microenvironment in tumor progression and therapeutic outcome has gained increasing attention. Cancer-associated fibroblasts (CAFs) have emerged as key players among stromal cells, owing to their abundance in most solid tumors and their diverse tumor-restraining/promoting roles. The interplay between tumor cells and neighboring CAFs takes place by both paracrine signals (cytokines, exosomes and metabolites) or by the multifaceted functions of the surrounding extracellular matrix. Here, we dissect the most recent identified mechanisms underlying CAF-mediated control of tumor progression and therapy resistance, which include induction of the epith…

0301 basic medicineCancer ResearchStromal cellEpithelial-Mesenchymal TransitionParacrine CommunicationAntineoplastic AgentsReviewBiologylcsh:RC254-28203 medical and health sciences0302 clinical medicineCancer-Associated FibroblastsCancer stem cellSettore MED/04 - PATOLOGIA GENERALENeoplasmsParacrine CommunicationTumor MicroenvironmentHumansEpithelial–mesenchymal transitionTumor microenvironmentCancer associated fibroblasts cancer stem cells extracellular matrix exosomes epithelial-to-mesenchymal transition.lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMicrovesiclesGene Expression Regulation Neoplastic030104 developmental biologyOncologyTumor progressionDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchDisease ProgressionMolecular MedicineCancer-Associated FibroblastsSignal Transduction
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Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

2017

Abstract Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal …

0301 basic medicineCancer ResearchStromal cellMyeloidMice TransgenicVascular RemodelingBiologyInbred C57BLTransgenicMice03 medical and health sciencesMyelogenousMyeloproliferative DisordersmedicineAnimalsHumansMyeloproliferative DisorderAnimals; Cell Proliferation; Humans; Mice; Mice Inbred C57BL; Mice Inbred CBA; Mice Transgenic; Myeloproliferative Disorders; Stromal Cells; Vascular Remodeling; Oncology; Cancer ResearchCell ProliferationMyeloproliferative DisordersAnimalStromal CellInbred CBANeutrophil extracellular trapsmedicine.diseaseMice Inbred C57BLHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureOncologyImmunologyMice Inbred CBABone marrowStromal CellsNucleophosminHuman
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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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Roles of TP53 in determining therapeutic sensitivity, growth, cellular senescence, invasion and metastasis.

2016

TP53 is a critical tumor suppressor gene that regulates cell cycle progression, apoptosis, cellular senescence and many other properties critical for control of normal cellular growth and death. Due to the pleiotropic effects that TP53 has on gene expression and cellular physiology, mutations at this tumor suppressor gene result in diverse physiological effects. T53 mutations are frequently detected in numerous cancers. The expression of TP53 can be induced by various agents used to treat cancer patients such as chemotherapeutic drugs and ionizing radiation. Radiation will induce Ataxia telangiectasia mutated (ATM) and other kinases that results in the phosphorylation and activation of TP53…

0301 basic medicineCancer Researchendocrine system diseasesMetastasimedicine.disease_causeMetastasisAntineoplastic AgentInvasionNeoplasmsTP53Neoplasm Metastasisbcl-2-Associated X ProteinAza CompoundProto-Oncogene ProteinApoptosis Regulatory ProteinbiologyCell CyclemiRMicroRNACell cycleCell biologyNeoplasm MetastasiGene Expression Regulation NeoplasticNutlin-3 chemosensitivityMdm2Molecular MedicineHumanSignal TransductionCyclin-Dependent Kinase Inhibitor p21Tumor suppressor genemiRsAntineoplastic AgentsCellular senescenceTP53; miRs; MDM2; Nutlin-3 chemosensitivity; Cellular senescence ; Invasion; Metastasis03 medical and health sciencesBcl-2-associated X proteinGeneticMDM2Proto-Oncogene ProteinsmicroRNAGeneticsmedicineHumansNeoplasm InvasivenessneoplasmsMolecular BiologyCell ProliferationNeoplasm InvasiveneAza CompoundsOncomirBridged Bicyclo Compounds HeterocyclicMicroRNAs030104 developmental biologyTumor progressionbiology.proteinNeoplasmTumor Suppressor Protein p53CarcinogenesisApoptosis Regulatory Proteins
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Identification of clinical phenotypes and related survival in patients with large hccs

2021

Background. Hepatocellular carcinoma (HCC) factors, especially maximum tumor diameter (MTD), tumor multifocality, portal vein thrombosis (PVT), and serum alpha-fetoprotein (AFP), influence survival. Aim. To examine patterns of tumor factors in large HCC patients. Methods. A database of large HCC patients was examined. Results. A multiple Cox proportional hazard model on death identified low serum albumin levels and the presence of PVT and multifocality, with each having a hazard ratio ≥2.0. All combinations of these three parameters were examined in relation to survival. Using univariate Cox analysis, the combination of albumin &gt

0301 basic medicineCancer Researchmedicine.medical_specialtyPVTSettore MED/12 - GASTROENTEROLOGIASerum albuminlcsh:RC254-282GastroenterologyArticle03 medical and health sciences0302 clinical medicineInternal medicineMedicinePlateletHCCneoplasmsSurvival ratePVT.biologybusiness.industryProportional hazards modelAlbuminHazard ratioSettore MED/09 - MEDICINA INTERNAAlbuminMultifocalityHCC; large; phenotypes; PVT; multifocality; albuminlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseasesPortal vein thrombosisAlbumin; HCC; Large; Multifocality; Phenotypes; PVTPhenotypesPhenotype030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinLargebusiness
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Portal vein infiltration in patients with hepatocellular carcinoma: The relevance of correct classification.

2017

e15651 Background: Portal vein invasion (PVI) is has a significant impact on the prognosis of patients with hepatocellular carcinoma (HCC). Patients with PVI are classified as stage C in the BCLC score and systemic therapy is recommended. Patients with minor PVI are frequently misclassified due to radiological challenges in determining malignant PVI or non-adherence to guidelines. The concept of resection or TACE in limited PVI is sometimes followed with the assumption of a negligible influence on survival. Aim of this study is the reevaluation of PVI and the analysis of the impact of a misclassification. Methods: 763 patients with HCC of a total of 1413 were extracted from the clinical re…

0301 basic medicineCancer Researchmedicine.medical_specialtyPathologybusiness.industryPortal veinmedicine.disease03 medical and health sciences030104 developmental biologyOncologyHepatocellular carcinomamedicineIn patientRadiologybusinessInfiltration (medical)Journal of Clinical Oncology
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