Search results for "Pathway"

showing 10 items of 1685 documents

Indomethacin Disrupts Autophagic Flux by Inducing Lysosomal Dysfunction in Gastric Cancer Cells and Increases Their Sensitivity to Cytotoxic Drugs

2018

AbstractNSAIDs inhibit tumorigenesis in gastrointestinal tissues and have been proposed as coadjuvant agents to chemotherapy. The ability of cancer epithelial cells to adapt to the tumour environment and to resist cytotoxic agents seems to depend on rescue mechanisms such as autophagy. In the present study we aimed to determine whether an NSAID with sensitizing properties such as indomethacin modulates autophagy in gastric cancer epithelial cells. We observed that indomethacin causes lysosomal dysfunction in AGS cells and promotes the accumulation of autophagy substrates without altering mTOR activity. Indomethacin enhanced the inhibitory effects of the lysosomotropic agent chloroquine on l…

0301 basic medicineCell SurvivalIndomethacinlcsh:MedicineAntineoplastic AgentsAdenocarcinomaArticle03 medical and health sciencesStomach NeoplasmsCell Line TumorLysosomeAutophagymedicineHumansCytotoxic T cellViability assayCytotoxicitylcsh:SciencePI3K/AKT/mTOR pathwayAnalysis of VarianceMultidisciplinaryCell DeathChemistryAnti-Inflammatory Agents Non-SteroidalAutophagylcsh:RChloroquineDrug SynergismOxaliplatin030104 developmental biologymedicine.anatomical_structureDrug Resistance NeoplasmApoptosisCancer cellCancer researchlcsh:QMacrolidesLysosomesScientific Reports
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Chemopreventive Property of Sencha Tea Extracts towards Sensitive and Multidrug-Resistant Leukemia and Multiple Myeloma Cells

2020

The popular beverage green tea possesses chemopreventive activity against various types of tumors. However, the effects of its chemopreventive effect on hematological malignancies have not been defined. In the present study, we evaluated antitumor efficacies of a specific green tea, sencha tea, on sensitive and multidrug-resistant leukemia and a panel of nine multiple myelomas (MM) cell lines. We found that sencha extracts induced cytotoxicity in leukemic cells and MM cells to different extents, yet its effect on normal cells was limited. Furthermore, sencha extracts caused G2/M and G0/G1 phase arrest during cell cycle progression in CCRF/CEM and KMS-12-BM cells, respectively. Specifically,…

0301 basic medicineCell Survivalnatural productsgreen tealcsh:QR1-502Cell morphologychemotherapyBiochemistryArticlelcsh:Microbiologyfunctional foodPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCell Line TumorHumansCytotoxicityMolecular BiologyProtein kinase BcatechinsPI3K/AKT/mTOR pathwaypolyphenolsCell ProliferationMembrane Potential MitochondrialLeukemiadrug resistanceTeaPlant ExtractsChemistryCell growthCell CycleNF-kappa BCell cycleAntineoplastic Agents PhytogenicDrug Resistance MultipleGene Expression Regulation Neoplastic030104 developmental biologyDrug Resistance NeoplasmApoptosisCell culture030220 oncology & carcinogenesisflavonoidsCancer researchmicroarray analysisMultiple MyelomaReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSignal TransductionBiomolecules
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WNT signaling modulates PD-L1 expression in the stem cell compartment of triple-negative breast cancer

2019

Triple-negative breast cancers (TNBCs) are characterized by a poor prognosis and lack of targeted treatments, and thus, new therapeutic strategies are urgently needed. Inhibitors against programmed death-1 (PD-1)/PD-1 ligand (PD-L1) have shown significant efficacy in various solid cancers, but their activity against TNBCs remains limited. Here, we report that human TNBCs molecularly stratified for high levels of PD-L1 (PD-L1High) showed significantly enriched expression of immune and cancer stemness pathways compared with those with low PD-L1 expression (PD-L1Low). In addition, the PD-L1High cases were significantly associated with a high stemness score (SSHigh) signature. TNBC cell lines g…

0301 basic medicineCell biologyCancer ResearchTriple Negative Breast NeoplasmImmunologyDown-RegulationTriple Negative Breast NeoplasmsArticleB7-H1 Antigen03 medical and health sciences0302 clinical medicineImmune systemStem CellCell Line TumorBiomarkers TumorGeneticsmedicineAnimalsHumansWnt Signaling PathwayMolecular BiologyTriple-negative breast cancerMice Inbred BALB CbiologyAnimalStem CellsCD44Wnt signaling pathwayCancerAldehyde Dehydrogenasemedicine.diseaseHyaluronan ReceptorUp-RegulationALDH1A1Hyaluronan Receptors030104 developmental biology030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleStem cellB7-H1 AntigenHumanOncogene
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CHK1 inhibitor sensitizes resistant colorectal cancer stem cells to nortopsentin

2021

Summary Limited therapeutic options are available for advanced colorectal cancer (CRC). Herein, we report that exposure to a neo-synthetic bis(indolyl)thiazole alkaloid analog, nortopsentin 234 (NORA234), leads to an initial reduction of proliferative and clonogenic potential of CRC sphere cells (CR-CSphCs), followed by an adaptive response selecting the CR-CSphC-resistant compartment. Cells spared by the treatment with NORA234 express high levels of CD44v6, associated with a constitutive activation of Wnt pathway. In CR-CSphC-based organoids, NORA234 causes a genotoxic stress paralleled by G2-M cell cycle arrest and activation of CHK1, driving the DNA damage repair of CR-CSphCs, regardless…

0301 basic medicineCell cycle checkpointColorectal cancerScienceSettore MED/50 - Scienze Tecniche Mediche Applicate02 engineering and technologyGenotoxic StressArticleMolecular Physiology03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALERabusertibmedicineClonogenic assayCancerMultidisciplinarybusiness.industryQWnt signaling pathwayDrugsCancerCell Biology021001 nanoscience & nanotechnologymedicine.disease030104 developmental biologyCancer researchSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioStem cell0210 nano-technologybusinesscolorectal cancer cancer stem cells alkaloids DNA damage repair CHK1.iScience
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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
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An actin network dispatches ciliary GPCRs into extracellular vesicles to modulate signaling

2017

Signaling receptors dynamically exit cilia upon activation of signaling pathways such as Hedgehog. Here, we find that when activated G protein-coupled receptors (GPCRs) fail to undergo BBSome-mediated retrieval from cilia back into the cell, these GPCRs concentrate into membranous buds at the tips of cilia before release into extracellular vesicles named ectosomes. Unexpectedly, actin and the actin regulators drebrin and myosin 6 mediate ectosome release from the tip of cilia. Mirroring signal-dependent retrieval, signal-dependent ectocytosis is a selective and effective process that removes activated signaling molecules from cilia. Congruently, ectocytosis compensates for BBSome defects as…

0301 basic medicineCell signalingBBSome*myosin 6*GPCR*exosomes*HedgehogBiologyKidneyGeneral Biochemistry Genetics and Molecular BiologyArticleCell LineReceptors G-Protein-Coupled03 medical and health sciencesExtracellular VesiclesMice0302 clinical medicine*BBSomeAnimalsHumans*ciliaCiliaReceptors SomatostatinHedgehog*actinActinG protein-coupled receptorCilium*extracellular vesiclesHedgehog signaling pathwayActinsCell biology030104 developmental biologyMicroscopy Electron ScanningSignal transduction*drebrin030217 neurology & neurosurgerySignal Transduction
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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
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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
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Evaluation of Planar-Cell-Polarity Phenotypes in Ciliopathy Mouse Mutant Cochlea

2016

In recent years, primary cilia have emerged as key regulators in development and disease by influencing numerous signaling pathways. One of the earliest signaling pathways shown to be associated with ciliary function was the non-canonical Wnt signaling pathway, also referred to as planar cell polarity (PCP) signaling. One of the best places in which to study the effects of planar cell polarity (PCP) signaling during vertebrate development is the mammalian cochlea. PCP signaling disruption in the mouse cochlea disrupts cochlear outgrowth, cellular patterning and hair cell orientation, all of which are affected by cilia dysfunction. The goal of this protocol is to describe the analysis of PCP…

0301 basic medicineCell signalingGeneral Chemical EngineeringStereocilia (inner ear)Cochlear ductBiologyGeneral Biochemistry Genetics and Molecular BiologyStereociliaMice03 medical and health sciencesHair Cells AuditorymedicineAnimalsCochleaGeneral Immunology and MicrobiologyGeneral NeuroscienceCiliumWnt signaling pathwayCell PolarityCochlear DuctEmbryo Mammalianmedicine.diseaseImmunohistochemistryCiliopathiesCochleaCell biologyDisease Models AnimalCiliopathyPhenotype030104 developmental biologymedicine.anatomical_structureMicroscopy Electron ScanningMedicinesense organsHair cellSignal TransductionJournal of Visualized Experiments
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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
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