Search results for "asm"

showing 10 items of 16598 documents

Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer.

2020

Cancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness and metastatic potential. Cancer cells adequately adapt cell metabolism and integrate several intracellular and redox signaling to promote cell survival in an inflammatory and hypoxic microenvironment in order to maintain/expand tumor phenotype. The administration of tyrosine kinase inhibitor (TKI) constitutes the recommended therapeutic strategy in different malignancies at advanced stages. There are important interrelationships between cell stress, redox status, mitochondrial function, metabolism and cellular signali…

0301 basic medicineCell deathCell signalingClinical BiochemistryPGC-1αApoptosisReview ArticleBiochemistryReceptor tyrosine kinase03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsAutophagyTumor MicroenvironmentHumansProtein kinase AProtein kinase Blcsh:QH301-705.5Protein Kinase InhibitorsPI3K/AKT/mTOR pathwaylcsh:R5-920biologyOrganic ChemistryMitochondria030104 developmental biologylcsh:Biology (General)Redox statusCancer cellbiology.proteinCancer researchEndoplasmic reticulum stressmTORSignal transductionlcsh:Medicine (General)Tyrosine kinaseProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryRedox biology
researchProduct

The Double-Edged Sword Profile of Redox Signaling: Oxidative Events As Molecular Switches in the Balance between Cell Physiology and Cancer.

2018

The intracellular redox state in the cell depends on the balance between the level of reactive oxygen species (ROS) and the activity of defensive systems including antioxidant enzymes. This balance is a dynamic process that can change in relation to many factors and/or stimuli induced within the cell. ROS production is derived from physiological metabolic events. For instance, mitochondria represent the major ROS sources during oxidative phosphorylation, but other systems, such as NADPH oxidase or specific enzymes in certain metabolisms, may account for ROS production as well. Whereas high levels of ROS perturb the cell environment, causing oxidative damage to biological macromolecules, low…

0301 basic medicineCell physiologyOxidative phosphorylationMitochondrionToxicologymedicine.disease_cause03 medical and health sciencesOxidative Stress ROS antioxidant systems0302 clinical medicineNeoplasmsmedicineAnimalsHumanschemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyChemistryNADPH OxidasesGeneral MedicineCell biology030104 developmental biology030220 oncology & carcinogenesisbiology.proteinSignal transductionReactive Oxygen SpeciesOxidation-ReductionIntracellularOxidative stressSignal TransductionChemical research in toxicology
researchProduct

Repurposing of Drugs Targeting YAP-TEAD Functions

2018

Drug repurposing is a fast and consolidated approach for the research of new active compounds bypassing the long streamline of the drug discovery process. Several drugs in clinical practice have been reported for modulating the major Hippo pathway’s terminal effectors, namely YAP (Yes1-associated protein), TAZ (transcriptional co-activator with PDZ-binding motif) and TEAD (transcriptional enhanced associate domains), which are directly involved in the regulation of cell growth and tissue homeostasis. Since this pathway is known to have many cross-talking phenomena with cell signaling pathways, many efforts have been made to understand its importance in oncology. Moreover, this could be rele…

0301 basic medicineCell signalingCell signalingCancer ResearchProtein-protein interactionsHippo pathwayDrug repurposingprotein-protein interactionsComputational biologyReviewBiologylcsh:RC254-28203 medical and health sciencesYAP-TEAD disruptioncell signalingRepurposingTissue homeostasisHippo signaling pathwaydrug repurposingEffectorCell growthDrug discoveryYap-tead disruptionlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensDrug repositioning030104 developmental biologyOncologyCell signaling; Drug repurposing; Hippo pathway; Protein-protein interactions; Yap-tead disruption; Oncology; Cancer ResearchCancers
researchProduct

Bioelectrical Signals and Ion Channels in the Modeling of Multicellular Patterns and Cancer Biophysics

2016

AbstractBioelectrical signals and ion channels are central to spatial patterns in cell ensembles, a problem of fundamental interest in positional information and cancer processes. We propose a model for electrically connected cells based on simple biological concepts: i) the membrane potential of a single cell characterizes its electrical state; ii) the long-range electrical coupling of the multicellular ensemble is realized by a network of gap junction channels between neighboring cells; and iii) the spatial distribution of an external biochemical agent can modify the conductances of the ion channels in a cell membrane and the multicellular electrical state. We focus on electrical effects …

0301 basic medicineCell signalingComputer scienceCèl·lulesQuantitative Biology::Tissues and OrgansCellElectrophysiological PhenomenaCell CommunicationModels BiologicalArticleBiophysical PhenomenaIon ChannelsMembrane PotentialsQuantitative Biology::Cell BehaviorCell membraneion transport03 medical and health sciences0302 clinical medicineNeoplasmsmedicineHumansbiological physicsIon channelIon transporterMembrane potentialMultidisciplinaryBiophysical PhenomenaGap junctionGap JunctionsBiofísicaElectrophysiological PhenomenaMulticellular organism030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisBiophysicsScientific Reports
researchProduct

EpCAM duality becomes this molecule in a new Dr. Jekyll and Mr. Hyde tale.

2018

EpCAM, known as an epithelial cell adhesion molecule, plays an essential role in cell adhesion, migration, metastasis and cell signalling. Rather than acting as an apoptosis antagonist, it induces cellular proliferation that impacts the cell cycle, and as a signalling transducer it uses and enhances the Wnt pathway, which is significantly relevant in cell renewal and cancer. EpCAM has become a marker of circulating tumour cells (CTCs) in lung cancer due to its specificity, and its high and stable expression level. Recent findings have allowed us to relearn and discover EpCAM again as a CSCs marker by demonstrating its role in human epithelial cancer progression. In line with this, the focus…

0301 basic medicineCell signalingEpithelial-Mesenchymal Transitionlaw.inventionMetastasis03 medical and health scienceschemistry.chemical_compound0302 clinical medicinelawCancer stem cellAntigens NeoplasmCell Line TumorNeoplasmsmedicineCell AdhesionAnimalsHumansCell Proliferationbusiness.industryWnt signaling pathwayCancerEpithelial cell adhesion moleculeHematologyCell cyclemedicine.diseaseEpithelial Cell Adhesion MoleculeNeoplastic Cells Circulating030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisCancer researchSuppressorbusinessSignal TransductionCritical reviews in oncology/hematology
researchProduct

Cyclic pentapeptide cRGDfK enhances the inhibitory effect of sunitinib on TGF-β1-induced epithelial-to-mesenchymal transition in human non-small cell…

2020

AbstractIn human lung cancer progression, the EMT process is characterized by the transformation of cancer cells into invasive forms that migrate to other organs. Targeting to EMT-related molecules is emerging as a novel therapeutic approach for the prevention of lung cancer cell migration and invasion. Traf2- and Nck-interacting kinase (TNIK) has recently been considered as an anti-proliferative target molecule to regulate the Wnt signaling pathway in several types of cancer cells. In the present study, we evaluated the inhibitory effect of a tyrosine kinase inhibitor sunitinib and the integrin-αVβ3targeted cyclic peptide (cRGDfK) on EMT in human lung cancer cells. Sunitinib strongly inhib…

0301 basic medicineCell signalingIntegrinsLung NeoplasmsProtein ExpressionCancer TreatmentSmad ProteinsSignal transductionLung and Intrathoracic TumorsTyrosine-kinase inhibitorAdenosine Triphosphate0302 clinical medicineCarcinoma Non-Small-Cell LungCatalytic DomainAntineoplastic Combined Chemotherapy ProtocolsMedicine and Health SciencesSunitinibWnt Signaling PathwayWNT Signaling CascadeMultidisciplinarySunitinibChemistryQRWnt signaling pathwaySignaling cascadesDrug SynergismExtracellular MatrixMolecular Docking SimulationOncology030220 oncology & carcinogenesisMedicineCellular Structures and OrganellesSignal transductionResearch Articlemedicine.drugCell biologySignal InhibitionEpithelial-Mesenchymal TransitionCell Survivalmedicine.drug_classScienceSMAD signalingProtein Serine-Threonine KinasesResearch and Analysis MethodsPeptides CyclicTransforming Growth Factor beta103 medical and health sciencesCell Line TumorGene Expression and Vector TechniquesCell AdhesionBiomarkers TumormedicineHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionMolecular Biology TechniquesLung cancerMolecular BiologyA549 cellMolecular Biology Assays and Analysis TechniquesBiology and life sciencesCancers and NeoplasmsIntegrin alphaVbeta3medicine.diseaseNon-Small Cell Lung Cancer030104 developmental biologyTGF-beta signaling cascadeA549 CellsTNIKCancer cellCancer researchPLOS ONE
researchProduct

Tissue factor at the crossroad of coagulation and cell signaling

2018

The tissue factor (TF) pathway plays a central role in hemostasis and thrombo-inflammatory diseases. Although structure-function relationships of the TF initiation complex are elucidated, new facets of the dynamic regulation of TF?s activities on cells continue to emerge. Cellular pathways that render TF non-coagulant participate in signaling of distinct TF complexes with associated proteases through the protease-activated receptor (PAR) family of G-protein coupled receptors. Additional coreceptors, including the endothelial protein C receptor (EPCR) and integrins, confer signaling specificity by directing subcellular localization and trafficking. We here review how TF is switchedbetween it…

0301 basic medicineCell signalingProteasesCIENCIAS MÉDICAS Y DE LA SALUDIntegrinInmunologíaFactor VIIaThromboplastin03 medical and health sciencesTissue factorPROTEINASE- ACTIVATED RECEPTORSNeoplasmsmedicineAnimalsHumansReceptor PAR-2Myeloid CellsHEMOSTASISProtease-activated receptorENDOTHELIAL PROTEIN C RECEPTORBlood CoagulationInflammationEndothelial protein C receptorInnate immune systembiologyChemistryEndothelial CellsThrombosisInflammasomeHematologyCell biologyTHROMBOSISMedicina Básica030104 developmental biologyFactor Xabiology.proteinPROTEIN DISULFIDE-ISOMERASESSignal Transductionmedicine.drugJournal of Thrombosis and Haemostasis
researchProduct

Direct estrogen receptor (ER) / HER family crosstalk mediating sensitivity to lumretuzumab and pertuzumab in ER+ breast cancer.

2017

Bidirectional cross talk between members of the human epidermal growth factor family of receptors (HER) and the estrogen receptor (ER) is believed to underlie resistance mechanisms that develop in response to treatment with anti-HER agents and endocrine therapy. We investigated the interaction between HER2, HER3 and the ER in vitro using human embryonic kidney cells transfected with human HER2, HER3, and ERα. We also investigated the additive efficacy of combination regimens consisting of anti-HER3 (lumretuzumab), anti-HER2 (pertuzumab), and endocrine (fulvestrant) therapy in vivo. Our data show that both HER2 and HER3 can directly complex with the ER and can mediate phosphorylation of the …

0301 basic medicineCell signalingReceptor ErbB-3Receptor ErbB-2Cancer TreatmentEstrogen receptorlcsh:MedicineSignal transductionBiochemistryMice0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsBreast TumorsMedicine and Health SciencesReceptorlcsh:Scienceskin and connective tissue diseasesMultidisciplinaryRemission InductionEndocrine TherapySignaling cascadesPrecipitation TechniquesTreatment OutcomeReceptors EstrogenOncology030220 oncology & carcinogenesisMonoclonalCell linesFemalePertuzumabBiological culturesmedicine.drugResearch ArticleAdultCell biologyMAPK signaling cascadesPaclitaxelBreast NeoplasmsAntibodies Monoclonal Humanized03 medical and health sciencesBreast cancerCell Line TumorBreast CancermedicineEndocrine systemAnimalsHumansImmunoprecipitationFulvestrantbusiness.industrylcsh:RHEK 293 cellsCancers and NeoplasmsBiology and Life SciencesEstrogensReceptor Cross-TalkLumretuzumabmedicine.diseaseXenograft Model Antitumor AssaysHormonesResearch and analysis methods030104 developmental biologyCancer researchlcsh:QbusinessPloS one
researchProduct

EphrinB2 repression through ZEB2 mediates tumour invasion and anti-angiogenic resistance.

2016

Diffuse invasion of the surrounding brain parenchyma is a major obstacle in the treatment of gliomas with various therapeutics, including anti-angiogenic agents. Here we identify the epi-/genetic and microenvironmental downregulation of ephrinB2 as a crucial step that promotes tumour invasion by abrogation of repulsive signals. We demonstrate that ephrinB2 is downregulated in human gliomas as a consequence of promoter hypermethylation and gene deletion. Consistently, genetic deletion of ephrinB2 in a murine high-grade glioma model increases invasion. Importantly, ephrinB2 gene silencing is complemented by a hypoxia-induced transcriptional repression. Mechanistically, hypoxia-inducible facto…

0301 basic medicineCell signalingScienceGeneral Physics and AstronomyRepressorDown-RegulationAngiogenesis InhibitorsEphrin-B2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleNeovascularization03 medical and health sciencesDownregulation and upregulationddc:570GliomamedicineGene silencingAnimalsHumansNeoplasm InvasivenessPsychological repressionZinc Finger E-box Binding Homeobox 2Regulation of gene expressionMice KnockoutMultidisciplinaryNeovascularization PathologicQGeneral ChemistryGliomamedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysCell HypoxiaCell biologyUp-RegulationBevacizumabGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyDrug Resistance Neoplasmmedicine.symptomNature communications
researchProduct

A novel 3D heterotypic spheroid model for studying extracellular vesicle-mediated tumour and immune cell communication

2017

Cancer-derived extracellular vesicles (EVs) have emerged as important mediators of tumour-host interactions, and they have been shown to exert various functional effects in immune cells. In most of the studies on human immune cells, EVs have been isolated from cancer cell culture medium or patients' body fluids and added to the immune cell cultures. In such a setting, the physiological relevance of the chosen EV concentration is unknown and the EV isolation method and the timing of EV administration may bias the results. In the current study we aimed to develop an experimental cell culture model to study EV-mediated effects in human T and B cells at conditions mimicking the tumour microenvi…

0301 basic medicineCell signalingT cellPopulationBiophysicsCell CommunicationBiochemistryExtracellular Vesicles03 medical and health sciences0302 clinical medicineImmune systemCell Line TumorSpheroids CellularmedicineHumanseducationMolecular Biologyeducation.field_of_studyChemistryNeoplasms ExperimentalCell BiologyExtracellular vesicleCoculture TechniquesCell biology030104 developmental biologymedicine.anatomical_structureCell culture030220 oncology & carcinogenesisCancer cellLeukocytes MononuclearCD8Biochemical and Biophysical Research Communications
researchProduct