Search results for "AntagomiRs"

showing 5 items of 5 documents

MiR-205-5p inhibition by locked nucleic acids impairs metastatic potential of breast cancer cells.

2018

AbstractMir-205 plays an important role in epithelial biogenesis and in mammary gland development but its role in cancer still remains controversial depending on the specific cellular context and target genes. We have previously reported that miR-205-5p is upregulated in breast cancer stem cells targeting ERBB pathway and leading to targeted therapy resistance. Here we show that miR-205-5p regulates tumorigenic properties of breast cancer cells, as well as epithelial to mesenchymal transition. Silencing this miRNA in breast cancer results in reduced tumor growth and metastatic spreading in mouse models. Moreover, we show that miR-205-5p knock-down can be obtained with the use of specific lo…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal Transitionmedicine.medical_treatmentAntagomirSettore MED/50 - Scienze Tecniche Mediche ApplicateImmunologyTransplantation HeterologousOligonucleotidesBreast NeoplasmsBiologyArticleTargeted therapy03 medical and health sciencesCellular and Molecular NeuroscienceMiceBreast cancerErbBCell MovementMice Inbred NODOligonucleotideCell Line TumormicroRNAmedicineGene silencingAnimalsHumansEpithelial–mesenchymal transitionlcsh:QH573-671Neoplasm MetastasisCell ProliferationAnimallcsh:CytologyCancerAntagomirsMicroRNACell Biologymedicine.diseaseNeoplasm MetastasiMicroRNAs030104 developmental biologyCancer researchFemaleStem cellBreast NeoplasmHumanCell deathdisease
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miRNA92a targets KLF2 and the phosphatase PTEN signaling to promote human T follicular helper precursors in T1D islet autoimmunity.

2016

Aberrant immune activation mediated by T effector cell populations is pivotal in the onset of autoimmunity in type 1 diabetes (T1D). T follicular helper (TFH) cells are essential in the induction of high-affinity antibodies, and their precursor memory compartment circulates in the blood. The role of TFH precursors in the onset of islet autoimmunity and signaling pathways regulating their differentiation is incompletely understood. Here, we provide direct evidence that during onset of islet autoimmunity, the insulin-specific target T-cell population is enriched with a C-X-C chemokine receptor type 5 (CXCR5)(+)CD4(+) TFH precursor phenotype. During onset of islet autoimmunity, the frequency o…

0301 basic medicineMaleReceptors CXCR5endocrine systemAdolescentPopulationPrimary Cell CultureKruppel-Like Transcription FactorsAutoimmunityMice TransgenicNodBiologymedicine.disease_causeCXCR5Autoimmunity03 medical and health sciencesIslets of LangerhansMicePhosphatidylinositol 3-Kinases0302 clinical medicineMice Inbred NODmedicineAnimalsHumansIL-2 receptorKlf2 ; Pten-pi3k Signaling ; T Follicular Helper Cells ; Mirna92a ; Type 1 DiabeteseducationChildPI3K/AKT/mTOR pathwayNOD miceAutoantibodiesgeographyeducation.field_of_studyMultidisciplinarygeography.geographical_feature_categoryForkhead Box Protein O1PTEN PhosphohydrolaseAntagomirsT-Lymphocytes Helper-InducerIsletMicroRNAs030104 developmental biologyDiabetes Mellitus Type 1Gene Expression RegulationImmunologyCancer researchFemale030215 immunologySignal Transduction
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A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes.

2018

Molecular checkpoints that trigger the onset of islet autoimmunity or progression to human type 1 diabetes (T1D) are incompletely understood. Using T cells from children at an early stage of islet autoimmunity without clinical T1D, we find that a microRNA181a (miRNA181a)-mediated increase in signal strength of stimulation and costimulation links nuclear factor of activated T cells 5 (NFAT5) with impaired tolerance induction and autoimmune activation. We show that enhancing miRNA181a activity increases NFAT5 expression while inhibiting FOXP3+ regulatory T cell (Treg) induction in vitro. Accordingly, Treg induction is improved using T cells from NFAT5 knockout (NFAT5ko) animals, whereas alter…

CD4-Positive T-Lymphocytes0301 basic medicineRegulatory T cellBiologymedicine.disease_causeAutoimmunityMice03 medical and health sciencesNFAT5microRNAImmunogeneticsmedicineAnimalsHumansPI3K/AKT/mTOR pathwaygeographygeography.geographical_feature_categoryNFATC Transcription FactorsAntagomirsFOXP3Forkhead Transcription FactorsGeneral MedicineIsletMice Mutant StrainsMicroRNAsTolerance inductionDiabetes Mellitus Type 1030104 developmental biologymedicine.anatomical_structureCancer researchFemale
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miR-20b and miR-451a Are Involved in Gastric Carcinogenesis through the PI3K/AKT/mTOR Signaling Pathway: Data from Gastric Cancer Patients, Cell Line…

2020

Gastric cancer (GC) is one of the most common and lethal gastrointestinal malignancies worldwide. Many studies have shown that development of GC and other malignancies is mainly driven by alterations of cellular signaling pathways. MicroRNAs (miRNAs) are small noncoding molecules that function as tumor-suppressors or oncogenes, playing an essential role in a variety of fundamental biological processes. In order to understand the functional relevance of miRNA dysregulation, studies analyzing their target genes are of major importance. Here, we chose to analyze two miRNAs, miR-20b and miR-451a, shown to be deregulated in many different malignancies, including GC. Deregulated expression of miR…

MaleCell signalingAntagonists & inhibitorsCaveolin 1ApoptosisCatalysisTuberous Sclerosis Complex 1 ProteinArticleInorganic Chemistrylcsh:ChemistryMicePhosphatidylinositol 3-KinasesStomach NeoplasmsCell Line TumormicroRNAPTENAnimalsHumans616.33-006.6 [udc]Physical and Theoretical ChemistryMolecular BiologyProtein kinase Blcsh:QH301-705.5SpectroscopyPI3K/AKT/mTOR pathwaybiologyTOR Serine-Threonine Kinasesgastric cancerOrganic ChemistryPTEN PhosphohydrolaseAntagomirsGeneral MedicineStomach neoplasms ; genetics ; MicroRNAs ; genetics ; Phosphoinositide-3 Kinase Inhibitors ; Phosphatidylinositol 3-Kinase ; metabolism ; Proto-Oncogene Proteins c-akt ; antagonists&inhibitors ; Proto-Oncogene Proteins c-akt ; metabolism ; TOR Serine-Threonine Kinases ; antagonists&inhibitors ; TOR Serine-Threonine Kinases ; metabolism ; Signal transduction ; drug effects ; Disease models animal ; MicemiR-451aComputer Science ApplicationsmicroRNAsDisease Models Animallcsh:Biology (General)lcsh:QD1-999biology.proteinCancer researchFemalemiR-20bSignal transductionCarrier ProteinsProto-Oncogene Proteins c-aktTXNIPSignal TransductionPI3K/AKT/mTOR signaling pathwayInternational Journal of Molecular Sciences
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Utilización de microRNAs como dianas terapéuticas en Distrofia Miotónica

2018

La distrofia miotónica tipo 1 (DM1) se debe a una expansión del triplete CTG en 3´UTR del gen DMPK, mientras que, la distrofia miotónica tipo 2 (DM2) se origina por la de la repetición CCTG en el intrón 1 del gen CNBP. Son dos enfermedades multisistémicas con manifestaciones patológicas en músculo esquelético (miotonia, degeneración y debilidad muscular), corazón (defectos en la conducción cardiaca) y sistema nervioso central. Los transcritos DMPK y CNBP mutantes se pliegan en horquillas que secuestran factores de splicing alternativo, principalmente Muscleblind-like 1 (MBNL1; y su parálogo MBNL2). La falta de la proteínas MBNL origina problemas en el splicing de transcritos musculares y co…

Terapia:CIENCIAS DE LA VIDA::Biología humana ::Genética humana [UNESCO]UNESCO::CIENCIAS DE LA VIDA::Biología humana ::Genética humanaAntagomiRsDistrofia MiotónicamicroRNAs
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