Search results for "G proteins"

showing 10 items of 992 documents

Dynamics and predicted drug response of a gene network linking dedifferentiation with β-catenin dysfunction in hepatocellular carcinoma

2019

Background & Aims Alterations of individual genes variably affect the development of hepatocellular carcinoma (HCC). Thus, we aimed to characterize the function of tumor-promoting genes in the context of gene regulatory networks (GRNs). Methods Using data from The Cancer Genome Atlas, from the LIRI-JP (Liver Cancer – RIKEN, JP project), and from our transcriptomic, transfection and mouse transgenic experiments, we identify a GRN which functionally links LIN28B-dependent dedifferentiation with dysfunction of β-catenin (CTNNB1). We further generated and validated a quantitative mathematical model of the GRN using human cell lines and in vivo expression data. Results We found that LIN28B and C…

0301 basic medicineBeta-cateninCarcinoma HepatocellularHepatocellular carcinomaLIN28BCellGene regulatory networkPrincipal component analysisMice TransgenicBiologyTransfectionTranscriptomeCohort Studies03 medical and health sciencesMice0302 clinical medicineMathematical modelmicroRNAmedicineAnimalsHumansGene Regulatory NetworksCTNNB1Genebeta CateninHepatologySequence Analysis RNALiver NeoplasmsGene regulatory networkRNA-Binding ProteinsHGF/MET pathwayMicroRNAHep G2 CellsHCCSModels TheoreticalPrognosisPersonalized medicinedigestive system diseases030104 developmental biologymedicine.anatomical_structureCancer researchSMARCA4biology.protein030211 gastroenterology & hepatologyTranscriptome
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Extracellular Vesicles Shed by Melanoma Cells Contain a Modified Form of H1.0 Linker Histone and H1.0 mRNA-binding Proteins

2016

Extracellular vesicles (EVs) are shed in the extracellular environment by both prokaryotes and eukaryotes. Although produced from both normal and cancer cells, malignant cells release a much higher amount of EVs, which also contain tumor-specific proteins and RNAs. We previously found that G26/24 oligodendroglioma cells shed EVs that contain the pro-apoptotic factors FasL and TRAIL1-2. Interestingly, G26/24 release, via EVs, extracellular matrix remodelling proteases3, and H1° histone protein4, and mRNA. To shed further light on the role of EVs in discarding proteins and mRNAs otherwise able to counteract proliferative signals, we studied a melanoma cell line (A375). We found that also thes…

0301 basic medicineCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueMYEF2ApoptosisRNA-binding proteinexosomesmembrane vesiclesReal-Time Polymerase Chain ReactionChromatography AffinityHistones03 medical and health sciencesH1.0 linker histone; RNA-binding proteins (RBPs); extracellular vesicles (EVs) membrane vesicles (MVs); exosomes; MYEF2Settore BIO/10 - BiochimicaTumor Cells CulturedHumansexosomeSecretionRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiamelanoma cell line (A375) myelin expression factor-2 (MYEF2)MelanomaTranscription factorCell ProliferationH1.0 linker histonebiologyReverse Transcriptase Polymerase Chain ReactionEXTRACELLULAR VESICLESRNA-Binding ProteinsRNACell DifferentiationArticlesCell biologyBlotCell Transformation Neoplastic030104 developmental biologyHistoneOncologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellbiology.proteinRNA-binding proteins (RBPs)extracellular vesicles (EVs) membrane vesicles (MVs)
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AP2α controls the dynamic balance between miR-126&126* and miR-221&222 during melanoma progression

2016

Accumulating evidences have shown the association between aberrantly expressed microRNAs (miRs) and cancer, where these small regulatory RNAs appear to dictate the cell fate by regulating all the main biological processes. We demonstrated the responsibility of the circuitry connecting the oncomiR-221&222 with the tumor suppressors miR-126&126∗ in melanoma development and progression. According to the inverse correlation between endogenous miR-221&222 and miR-126&126∗, respectively increasing or decreasing with malignancy, their enforced expression or silencing was sufficient for a reciprocal regulation. In line with the opposite roles of these miRs, protein analyses confirmed the reverse ex…

0301 basic medicineCancer ResearchCellular differentiationSettore MED/08 - Anatomia Patologicagrowth-factorCell fate determinationBiologyFatty Acid-Binding ProteinsBioinformaticsap-2 transcription factorlaw.inventioncutaneous melanoma03 medical and health sciencesMolecular Biology; Cancer Research; Genetics0302 clinical medicinelawTranscription (biology)Cell Line TumormicroRNAGeneticsmedicineHumansGene silencingMelanomaMolecular BiologyPsychological repressionsquamous-cell carcinoma; ap-2 transcription factor; cutaneous melanoma; growth-factor; metastatic melanoma; terminal fragment; cancer-cells; tumor-growth; mir-126; methylationMelanomaCell Differentiationsquamous-cell carcinomatumor-growthmedicine.diseaseMicroRNAscancer-cells030104 developmental biologyterminal fragmentmir-126030220 oncology & carcinogenesisDisease ProgressionCancer researchSuppressorOriginal Articlemethylationmetastatic melanomaOncogene
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In silico RNA-seq and experimental analyses reveal the differential expression and splicing of EPDR1 and ZNF518B genes in relation to KRAS mutations …

2016

Several drugs used for the treatment of colorectal cancer (CRC) are targeted at the epidermal growth factor receptor, but mutations in genes of the RAS family cause resistance to these drugs. Thus, extensive research is being carried out to counterbalance this resistance. The G13D mutation of KRAS is common in humans, and we previously reported that this mutation results in the epigenetic modification of hnRNP proteins, involved in RNA splicing. As aberrant splicing often results in oncogenicity, the present study aimed to identify the genes which show altered splicing patterns in connection with the G13D KRAS mutation. To accomplish this, we first carried out an in silico analysis of RNA-s…

0301 basic medicineCancer ResearchIn silicoMutation MissenseGene ExpressionNerve Tissue ProteinsBiologymedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicinemedicineHumansProtein IsoformsComputer SimulationEpigeneticsGeneGeneticsMutationBase SequenceModels GeneticSequence Analysis RNAAlternative splicingGeneral Medicinedigestive system diseasesNeoplasm ProteinsDNA-Binding ProteinsAlternative Splicing030104 developmental biologyOncology030220 oncology & carcinogenesisRNA splicingCancer researchKRASCarcinogenesisColorectal NeoplasmsOncology reports
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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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Epigenetic Silencing of CDR1as Drives IGF2BP3-Mediated Melanoma Invasion and Metastasis.

2018

Summary Metastasis is the primary cause of death of cancer patients. Dissecting mechanisms governing metastatic spread may uncover important tumor biology and/or yield promising therapeutic insights. Here, we investigated the role of circular RNAs (circRNA) in metastasis, using melanoma as a model aggressive tumor. We identified silencing of cerebellar degeneration-related 1 antisense (CDR1as), a regulator of miR-7, as a hallmark of melanoma progression. CDR1as depletion results from epigenetic silencing of LINC00632, its originating long non-coding RNA (lncRNA) and promotes invasion in vitro and metastasis in vivo through a miR-7-independent, IGF2BP3-mediated mechanism. Moreover, CDR1as le…

0301 basic medicineCancer ResearchRegulatorNerve Tissue ProteinsBiologyAutoantigensArticleMetastasisEpigenesis Genetic03 medical and health sciences0302 clinical medicinemedicineGene silencingHumansEnhancer of Zeste Homolog 2 ProteinNeoplasm InvasivenessRNA AntisenseGene SilencingNeoplasm MetastasisMelanomaMelanomaEZH2RNACancerRNA-Binding ProteinsRNA Circularmedicine.diseasePhospholipid Hydroperoxide Glutathione PeroxidasePrognosisMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchbiology.proteinRNA Long NoncodingPRC2Cancer cell
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2-Methoxyestradiol Affects Mitochondrial Biogenesis Pathway and Succinate Dehydrogenase Complex Flavoprotein Subunit A in Osteosarcoma Cancer Cells.

2017

Background/aim Dysregulation of mitochondrial pathways is implicated in several diseases, including cancer. Notably, mitochondrial respiration and mitochondrial biogenesis are favored in some invasive cancer cells, such as osteosarcoma. Hence, the aim of the current work was to investigate the effects of 2-methoxyestradiol (2-ME), a potent anticancer agent, on the mitochondrial biogenesis of osteosarcoma cells. Materials and methods Highly metastatic osteosarcoma 143B cells were treated with 2-ME separately or in combination with L-lactate, or with the solvent (non-treated control cells). Protein levels of α-syntrophin and peroxisome proliferator-activated receptor gamma, coactivator 1 alph…

0301 basic medicineCancer ResearchSIRT3Protein subunitSDHAMuscle ProteinsAntineoplastic AgentsMolecular Dynamics SimulationBiochemistryElectron Transport Complex IV03 medical and health sciences0302 clinical medicineGeneticSettore BIO/10 - BiochimicaCell Line TumorSirtuin 3CoactivatorGeneticsHumansMolecular BiologyOsteosarcomaOrganelle BiogenesisbiologyEstradiolSettore BIO/16 - Anatomia UmanaChemistryElectron Transport Complex IICalcium-Binding ProteinsMembrane ProteinsPeroxisomeMitochondrial biogenesiPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biology2-MethoxyestradiolMitochondriaSuccinate dehydrogenaseMolecular Docking Simulation030104 developmental biologyMitochondrial biogenesisSettore CHIM/03 - Chimica Generale E Inorganica030220 oncology & carcinogenesisSirtuinCancer cellbiology.proteinResearch ArticleCancer genomicsproteomics
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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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Ligand-dependent Hedgehog pathway activation in Rhabdomyosarcoma : the oncogenic role of the ligands

2017

Altres ajuts: This work was supported by grants from Institut Català d'Oncologia (ICO), Instituto de Salud Carlos III (RTICC-RD12/0036/0016, /0020, /0035, /0057; and PI14/00647), Fundació A BOSCH, Fundació Amics Joan Petit, ajuts predoctorals del VHIR and RIS3CAT grants COMRDI15-1-0014 (ACCIÓ and FEDER). Altres ajuts: FEDER/COMRDI15-1-0014 Rhabdomyosarcoma (RMS) is the most common type of soft tissue sarcoma in children. The Hedgehog (HH) pathway is known to develop an oncogenic role in RMS. However, the molecular mechanism that drives activation of the pathway in RMS is not well understood. The expression of HH ligands was studied by qPCR, western blot and immunohistochemistry. Functional …

0301 basic medicineCancer ResearchsarcomaCarcinogenesisVismodegibRhabdomyosarcoma; Hedgehog; vismodegib; UPR; TRIB3; sarcoma; cancerVismodegib610ApoptosisMice SCIDUPRLigandsMice03 medical and health sciences0302 clinical medicineCell MovementvismodegibRhabdomyosarcomaTumor Cells CulturedmedicinecancerAnimalsHumansHedgehog ProteinsAutocrine signallingRhabdomyosarcomaHedgehogCell ProliferationCancerChemistryTRIB3Sarcomamedicine.diseaseXenograft Model Antitumor AssaysHedgehog signaling pathway3. Good health030104 developmental biologyOncology030220 oncology & carcinogenesisUnfolded protein responseCancer researchFemaleSignal transductionTranslational TherapeuticsSmoothenedHedgehogSignal TransductionTranscription Factorsmedicine.drug
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Opposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma

2018

Recurrent mutations in chromatin modifiers are specifically prevalent in adolescent or adult patients with Sonic hedgehog-associated medulloblastoma (SHH MB). Here, we report that mutations in the acetyltransferase CREBBP have opposing effects during the development of the cerebellum, the primary site of origin of SHH MB. Our data reveal that loss of Crebbp in cerebellar granule neuron progenitors (GNPs) during embryonic development of mice compromises GNP development, in part by downregulation of brain-derived neurotrophic factor (Bdnf). Interestingly, concomitant cerebellar hypoplasia was also observed in patients with Rubinstein-Taybi syndrome, a congenital disorder caused by germline mu…

0301 basic medicineCerebellumCrebbp protein mousemetabolism [Cerebellar Neoplasms]acetyltransferase; cerebellum; CREBBP; development; Rubinstein-Taybi syndrome; SHH medulloblastomagenetics [Hedgehog Proteins]MiceNeurotrophic factorsmetabolism [CREB-Binding Protein]Mice KnockoutNeuronsRubinstein-Taybi Syndromepathology [Rubinstein-Taybi Syndrome]CREBBPCREB-Binding ProteinPhenotypegenetics [CREB-Binding Protein]3. Good healthpathology [Cerebellar Neoplasms]acetyltransferasePhenotypemedicine.anatomical_structuregenetics [Rubinstein-Taybi Syndrome]Femalemetabolism [Hedgehog Proteins]Signal TransductionSHH medulloblastomaAdultcerebellumBiologyGeneral Biochemistry Genetics and Molecular BiologyCREBBP; Rubinstein-Taybi syndrome; SHH medulloblastoma; acetyltransferase; cerebellum; development.03 medical and health sciencesGermline mutationAcetyltransferasesmetabolism [Medulloblastoma]medicineAnimalsHumansgenetics [Cerebellar Neoplasms]Hedgehog Proteinsddc:610Cerebellar NeoplasmsdevelopmentMolecular BiologyMedulloblastomaRubinstein–Taybi syndromegenetics [Medulloblastoma]metabolism [Rubinstein-Taybi Syndrome]pathology [Medulloblastoma]Cell Biologymedicine.disease030104 developmental biologyMutationphysiology [CREB-Binding Protein]Cancer researchSHH protein humanCerebellar hypoplasia (non-human)metabolism [Acetyltransferases]CREBBP protein humanMedulloblastomaDevelopmental BiologyCongenital disorderDevelopmental Cell
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