Search results for "Regulatory"

showing 10 items of 740 documents

Expression of regulatory genes in the embryonic brain of a lizard and implications for understanding pallial organization and evolution

2017

The comparison of gene expression patterns in the embryonic brain of mouse and chicken is being essential for understanding pallial organization. However, the scarcity of gene expression data in reptiles, crucial for understanding evolution, makes it difficult to identify homologues of pallial divisions in different amniotes. We cloned and analyzed the expression of the genes Emx1, Lhx2, Lhx9, and Tbr1 in the embryonic telencephalon of the lacertid lizard Psammodromus algirus. The comparative expression patterns of these genes, critical for pallial development, are better understood when using a recently proposed six-part model of pallial divisions. The lizard medial pallium, expressing all…

0301 basic medicineCalbindinsArcopalliumLIM-Homeodomain ProteinsEMX1ReptileBiologyCalbindinLhx903 medical and health sciencesforebrain evolutiontranscription factorsmedicineTranscription factorsAnimalsDlx2Research ArticlesHomeodomain ProteinsNeocortexCerebrumGeneral NeuroscienceDLX2RRID AB_10000340BrainGene Expression Regulation DevelopmentalLizardsBiological Evolutionreptile030104 developmental biologymedicine.anatomical_structureCalbindin 1Developmental regulatory genesbiology.proteinNidopalliumEmx1TBR1developmental regulatory genesT-Box Domain ProteinsNeuroscienceForebrain evolutionResearch Article
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Caloric Restriction Mimetics Enhance Anticancer Immunosurveillance

2016

International audience; Caloric restriction mimetics (CRMs) mimic the biochemical effects of nutrient deprivation by reducing lysine acetylation of cellular proteins, thus triggering autophagy. Treatment with the CRM hydroxycitrate, an inhibitor of ATP citrate lyase, induced the depletion of regulatory T cells (which dampen anticancer immunity) from autophagy-competent, but not autophagy-deficient, mutant KRAS-induced lung cancers in mice, thereby improving anticancer immunosurveillance and reducing tumor mass. Short-term fasting or treatment with several chemically unrelated autophagy-inducing CRMs, including hydroxycitrate and spermidine, improved the inhibition of tumor growth by chemoth…

0301 basic medicineCancer ResearchATP citrate lyaseSpermidineBariatric SurgeryimmunosurveillanceT-Lymphocytes RegulatoryAutophagy-Related Protein 5[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compoundMiceregulatory T cellCitrates3. Good healthImmunogenic Cell-DeathImmunosurveillancemedicine.anatomical_structureOncologyBiochemistryDifferentiationembryonic structuresImmunogenic cell deathIn-VivoHumanRegulatory T cell[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyDietary RestrictionNOProto-Oncogene Proteins p21(ras)03 medical and health sciencesMonitoring ImmunologicIn vivoCell Line TumormedicineAutophagyAnimalsHumanscancerChemotherapyBreast-CancerCaloric Restrictioncancer; chemotherapy immunosurveillance regulatory T cellAnimal[ SDV.BC ] Life Sciences [q-bio]/Cellular Biologyregulatory T&nbspAutophagyfungiNeoplasms ExperimentalcellSpermidineMethotrexate030104 developmental biologychemistryAcetylationMutationCancer researchCitrateNeoplasm Transplantation
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Common extracellular matrix regulation of myeloid cell activity in the bone marrow and tumor microenvironments

2017

The complex interaction between cells undergoing transformation and the various stromal and immunological cell components of the tumor microenvironment (TME) crucially influences cancer progression and diversification, as well as endowing clinical and prognostic significance. The immunosuppression characterizing the TME depends on the recruitment and activation of different cell types including regulatory T cells, myeloid-derived suppressor cells, and tumor-associated macrophages. Less considered is the non-cellular component of the TME. Here, we focus on the extracellular matrix (ECM) regulatory activities that, within the TME, actively contribute to many aspects of tumor progression, acti…

0301 basic medicineCancer ResearchCell typeStromal cellMyeloidCarcinogenesisImmunologyBiology03 medical and health sciencesBone MarrowNeoplasmsmedicineImmune ToleranceImmunology and AllergyAnimalsHumansMyeloid-Derived Suppressor CellCarcinogenesiTumor microenvironmentAnimalMyeloid-Derived Suppressor CellsHematopoietic stem cellSPARCBone marrow nicheExtracellular matrixCell biology030104 developmental biologymedicine.anatomical_structureRegulatory myeloid suppressor cellOncologyTumor microenvironmentTumor progressionMyeloid-derived Suppressor CellBone marrow niche; Extracellular matrix; Regulatory myeloid suppressor cells; SPARC; Tumor microenvironment; Animals; Bone Marrow; Carcinogenesis; Extracellular Matrix; Humans; Immune Tolerance; Myeloid-Derived Suppressor Cells; Neoplasms; Tumor Escape; Tumor MicroenvironmentNeoplasmTumor Escapesense organsBone marrowHuman
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The phospholipase DDHD1 as a new target in colorectal cancer therapy

2018

Background Our previous study demonstrates that Citrus-limon derived nanovesicles are able to decrease colon cancer cell viability, and that this effect is associated with the downregulation of the intracellular phospholipase DDHD domain-containing protein 1 (DDHD1). While few studies are currently available on the contribution of DDHD1 in neurological disorders, there is no information on its role in cancer. This study investigates the role of DDHD1 in colon cancer. Methods DDHD1 siRNAs and an overexpression vector were transfected into colorectal cancer and normal cells to downregulate or upregulate DDHD1 expression. In vitro and in vivo assays were performed to investigate the functional…

0301 basic medicineCancer ResearchColorectal cancerApoptosisMiceSettore BIO/13 - Biologia ApplicataGene Regulatory NetworksMolecular Targeted TherapyCitrus-limon nanovesicleTransfectionlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Oncology; Cancer ResearchOncologyPhospholipasesCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Animals; Antineoplastic Agents; Apoptosis; Cell Line Tumor; Cell Proliferation; Colorectal Neoplasms; Computational Biology; Disease Models Animal; Female; Gene Expression Profiling; Gene Ontology; Gene Regulatory Networks; Gene Silencing; Humans; MAP Kinase Signaling System; Mice; Phospholipases; Signal Transduction; Xenograft Model Antitumor Assays; Biomarkers Tumor; Molecular Targeted TherapyFemaleColorectal NeoplasmsSignal TransductionMAP Kinase Signaling SystemAntineoplastic Agentslcsh:RC254-282Citrus-limon nanovesicles03 medical and health sciencesDownregulation and upregulationIn vivoCell Line TumorBiomarkers TumormedicineAnimalsHumansGene silencingGene SilencingPhospholipase DDHD1Cell Proliferationbusiness.industryCell growthGene Expression ProfilingResearchComputational BiologyCancermedicine.diseaseXenograft Model Antitumor AssaysColorectal cancerDisease Models AnimalGene Ontology030104 developmental biologyApoptosisCancer researchbusiness
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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Comprehensive translational control of tyrosine kinase expression by upstream open reading frames

2016

Post-transcriptional control has emerged as a major regulatory event in gene expression and often occurs at the level of translation initiation. Although overexpression or constitutive activation of tyrosine kinases (TKs) through gene amplification, translocation or mutation are well-characterized oncogenic events, current knowledge about translational mechanisms of TK activation is scarce. Here, we report the presence of translational cis-regulatory upstream open reading frames (uORFs) in the majority of transcript leader sequences of human TK mRNAs. Genetic ablation of uORF initiation codons in TK transcripts resulted in enhanced translation of the associated downstream main protein-codin…

0301 basic medicineCancer ResearchFive prime untranslated regionKozak consensus sequenceShort CommunicationBiologymedicine.disease_causeProto-Oncogene MasGene Expression Regulation Enzymologic03 medical and health sciencesOpen Reading FramesEukaryotic translationUpstream open reading frameGeneticsmedicineHumansGene Regulatory NetworksMolecular BiologyGeneticsMutationGene Expression ProfilingTranslation (biology)Protein-Tyrosine KinasesOpen reading frame030104 developmental biologyHEK293 CellsProtein BiosynthesisHuman genomeHeLa Cells
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HMG-CoA reductase promotes protein prenylation and therefore is indispensible for T-cell survival.

2017

AbstractStatins are a well-established family of drugs that lower cholesterol levels via the competitive inhibition of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). In addition, the pleiotropic anti-inflammatory effects of statins on T cells make them attractive as therapeutic drugs in T-cell-driven autoimmune disorders. Since statins do not exclusively target HMGCR and thus might have varying effects on different cell types, we generated a new mouse strain allowing for the tissue-specific deletion of HMGCR. Deletion of HMGCR expression in T cells led to a severe decrease in their numbers with the remaining cells displaying an activated phenotype, with an increased pro…

0301 basic medicineCancer ResearchGeranylgeranyl pyrophosphateCell SurvivalT cellT-LymphocytesImmunologyProtein PrenylationMevalonic AcidCell CountMevalonic acidLymphocyte ActivationT-Lymphocytes Regulatory03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinePolyisoprenyl PhosphatesmedicineAnimalsbiologyCell DeathIntegrasesCholesterolCell BiologyHydroxymethylglutaryl-CoA reductaseCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurePhenotypeBiochemistrychemistryHMG-CoA reductasebiology.proteinProtein prenylationlipids (amino acids peptides and proteins)Hydroxymethylglutaryl CoA ReductasesOriginal ArticleMevalonate pathway030217 neurology & neurosurgeryGene DeletionCell deathdisease
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Concepts to Target MYC in Pancreatic Cancer.

2016

Abstract Current data suggest that MYC is an important signaling hub and driver in pancreatic ductal adenocarcinoma (PDAC), a tumor entity with a strikingly poor prognosis. No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792–8. ©2016 AACR.

0301 basic medicineCancer ResearchPoor prognosisPancreatic ductal adenocarcinomaendocrine system diseasesGene regulatory networkAntineoplastic AgentsBiologymedicine.disease_causeBioinformaticsProto-Oncogene Proteins c-myc03 medical and health sciencesPancreatic cancerCarcinomamedicineAnimalsHumansGene Regulatory NetworksMolecular Targeted TherapyProtein Kinase InhibitorsCancerGenetic Variationmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticPancreatic Neoplasms030104 developmental biologyOncologyCarrier proteinCancer researchKRASCarrier ProteinsCarcinoma Pancreatic DuctalProtein BindingSignal TransductionMolecular cancer therapeutics
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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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Rational Combination of Parvovirus H1 With CTLA-4 and PD-1 Checkpoint Inhibitors Dampens the Tumor Induced Immune Silencing

2019

The recent therapeutic success of immune checkpoint inhibitors in the treatment of advanced melanoma highlights the potential of cancer immunotherapy. Oncolytic virus-based therapies may further improve the outcome of these cancer patients. A human ex vivo melanoma model was used to investigate the oncolytic parvovirus H-1 (H-1PV) in combination with ipilimumab and/or nivolumab. The effect of this combination on activation of human T lymphocytes was demonstrated. Expression of CTLA-4, PD-1, and PD-L1 immune checkpoint proteins was upregulated in H-1PV-infected melanoma cells. Nevertheless, maturation of antigen presenting cells such as dendritic cells was triggered by H-1PV infected melanom…

0301 basic medicineCancer ResearchRegulatory T cellmedicine.medical_treatmentIpilimumablcsh:RC254-28203 medical and health sciences0302 clinical medicineimmune cellsCancer immunotherapymedicinemelanomaCytotoxic T cellipilimumabAntigen-presenting cellOriginal Researchnivolumabbusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensImmune checkpointH-1PV030104 developmental biologymedicine.anatomical_structureOncologyCTLA-4030220 oncology & carcinogenesisCancer researchimmunotherapyNivolumabbusinessmedicine.drugFrontiers in Oncology
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