Search results for "RCI"

showing 10 items of 16009 documents

Noncanonical GLI1 signaling promotes stemness features and in vivo growth in lung adenocarcinoma

2016

Aberrant Hedgehog/GLI signaling has been implicated in a diverse spectrum of human cancers, but its role in lung adenocarcinoma (LAC) is still under debate. We show that the downstream effector of the Hedgehog pathway, GLI1, is expressed in 76% of LACs, but in roughly half of these tumors, the canonical pathway activator, Smoothened, is expressed at low levels, possibly owing to epigenetic silencing. In LAC cells including the cancer stem cell compartment, we show that GLI1 is activated noncanonically by MAPK/ERK signaling. Different mechanisms can trigger the MAPK/ERK/GLI1 cascade including KRAS mutation and stimulation of NRP2 by VEGF produced by the cancer cells themselves in an autocrin…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsPyridinesPyridineMitogen-Activated Protein Kinase KinaseMice SCIDMiceCarcinoma Non-Small-Cell LungRNA Small InterferingNon-Small-Cell LungMolecular Biology; Genetics; Cancer ResearchTumorbiologyintegumentary systemHedgehog signaling pathwayCell biologyNeoplastic Stem CellsFemaleRNA InterferenceOriginal ArticleHumanXenograft Model Antitumor AssayAdenocarcinomaSCIDSmall InterferingZinc Finger Protein GLI1Cell LineProto-Oncogene Proteins p21(ras)Adenocarcinoma; Animals; Carcinoma Non-Small-Cell Lung; Cell Line Tumor; Female; Humans; Lung Neoplasms; Mice; Mice SCID; Mitogen-Activated Protein Kinase Kinases; Neoplastic Stem Cells; Neuropilin-2; Proto-Oncogene Proteins p21(ras); Pyridines; Pyrimidines; RNA Interference; RNA Small Interfering; Xenograft Model Antitumor Assays; Zinc Finger Protein GLI1; Molecular Biology; Genetics; Cancer Research03 medical and health sciencesParacrine signallingGeneticSettore MED/04 - PATOLOGIA GENERALEstem cellsCancer stem cellGLI1Cell Line TumorGeneticsAnimalsHumansAutocrine signallingMolecular BiologyMitogen-Activated Protein Kinase KinasesSettore MED/06 - ONCOLOGIA MEDICAAnimalCarcinomaXenograft Model Antitumor AssaysNeuropilin-2Lung Neoplasmlung cancer030104 developmental biologyPyrimidinesPyrimidineCancer cellbiology.proteinRNANeoplastic Stem CellSmoothened
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Autocrine CCL5 Effect Mediates Trastuzumab Resistance by ERK Pathway Activation in HER2-Positive Breast Cancer.

2020

Abstract HER2-positive breast cancer is currently managed with chemotherapy in combination with specific anti-HER2 therapies, including trastuzumab. However, a high percentage of patients with HER2-positive tumors do not respond to trastuzumab (primary resistance) or either recur (acquired resistance), mostly due to molecular alterations in the tumor that are either unknown or undetermined in clinical practice. Those alterations may cause the tumor to be refractory to treatment with trastuzumab, promoting tumor proliferation and metastasis. Using continued exposure of a HER2-positive cell line to trastuzumab, we generated a model of acquired resistance characterized by increased expression …

0301 basic medicineMAPK/ERK pathwayCancer ResearchMAP Kinase Signaling SystemReceptor ErbB-2medicine.medical_treatmentMice NudeApoptosisBreast NeoplasmsCCL5Metastasis03 medical and health sciencesMice0302 clinical medicineBreast cancerAntineoplastic Agents ImmunologicalTrastuzumabmedicineBiomarkers TumorTumor Cells CulturedGene silencingAnimalsHumansskin and connective tissue diseasesAutocrine signallingneoplasmsChemokine CCL5Neoadjuvant therapyCell Proliferationbusiness.industryGene Expression ProfilingTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticAutocrine Communication030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemalebusinessmedicine.drugMolecular cancer therapeutics
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RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1 and TP53 pathways and regulatory miRs as therapeutic targets in hepatocellular carcinoma

2019

Introduction: Hepatocellular carcinoma (HCC) is a significant problem globally because of viral infections and the increasing incidence of obesity and fatty liver disease. However, it is difficult to treat because its inherent genetic heterogeneity results in activation of numerous signaling pathways. Kinases have been targeted for decades with varying results, but the development of therapeutic resistance is a major challenge. Areas covered: The key roles of the RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1, TP53 microRNAs (miRs) as therapeutic targets are discussed and we suggests novel approaches for targeting miRs or their downstream targets to combat HCC. We performed literature searches using…

0301 basic medicineMAPK/ERK pathwayCarcinoma HepatocellularHepatocellular carcinmamedicine.medical_treatmentClinical BiochemistryAntineoplastic AgentsmTORC1signal transduction inhibitorsTargeted therapy03 medical and health sciences0302 clinical medicineDrug DiscoverymicroRNAmedicinePTENAnimalsHumanscancerMolecular Targeted TherapyTP53HCCRAS/RAF/MEK/ERKProtein kinase BPI3K/AKT/mTOR pathwaymiRNAPharmacologybiologybusiness.industryKinaseLiver NeoplasmsMirhepatocellular carcinomatargeted therapyGene Expression Regulation NeoplasticMicroRNAssignal transduction inhibitor030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbiology.proteinCancer researchMolecular MedicinePI3K/PTEN/AKTbusinessSignal Transduction
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Therapeutic resistance in breast cancer cells can result from deregulated EGFR signaling

2020

The epidermal growth factor receptor (EGFR) interacts with various downstream molecules including phospholipase C (PLC)/protein kinase C (PKC), Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/GSK-3, Jak/STAT and others. Often these pathways are deregulated in human malignancies such as breast cancer. Various therapeutic approaches to inhibit the activity of EGFR family members including small molecule inhibitors and monoclonal antibodies (MoAb) have been developed. A common problem with cancer treatments is the development of drug-resistance. We examined the effects of a conditionally-activated EGFR (v-Erb-B:ER) on the resistance of breast cancer cells to commonly used chemotherapeutic drugs such as doxorub…

0301 basic medicineMAPK/ERK pathwayEGFRvIIICancer ResearchEGFREstrogen receptorAntineoplastic AgentsBreast Neoplasms03 medical and health sciences0302 clinical medicineBreast cancerBreast cancerCell Line TumorGeneticsHumansMedicinePTENEpidermal growth factor receptorskin and connective tissue diseasesMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologybusiness.industryCancermedicine.diseaseErbB Receptors030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisDrug resistancebiology.proteinCancer researchMolecular MedicineFemalebusinessSignal TransductionV-Erb-B
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Mycobacterium tuberculosis Rv2145c Promotes Intracellular Survival by STAT3 and IL-10 Receptor Signaling

2021

Although Mycobacterium tuberculosis (Mtb) is an intracellular pathogen in phagocytic cells, the factors and mechanisms by which they invade and persist in host cells are still not well understood. Characterization of the bacterial proteins modulating macrophage function is essential for understanding tuberculosis pathogenesis and bacterial virulence. Here we investigated the pathogenic role of the Rv2145c protein in stimulating IL-10 production. We first found that recombinant Rv2145c stimulated bone marrow-derived macrophages (BMDMs) to secrete IL-10, IL-6 and TNF-α but not IL-12p70 and to increase the expression of surface molecules through the MAPK, NF-κB, and TLR4 pathways and enhanced …

0301 basic medicineMAPK/ERK pathwayImmunologyMicrobiologySTAT3Mycobacterium tuberculosis03 medical and health sciencesRv2145c0302 clinical medicineImmunology and AllergyMacrophageSecretionOriginal Researchpathogenic rolebiologyMycobacterium smegmatisMycobacterium tuberculosisRC581-607biology.organism_classificationInterleukin 10030104 developmental biology030220 oncology & carcinogenesisIL-10TLR4Immunologic diseases. AllergyIntracellularFrontiers in Immunology
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Modulation of the TGF-β1-induced epithelial to mesenchymal transition (EMT) mediated by P1 and P2 purine receptors in MDCK cells

2017

Epithelial to mesenchymal transition (EMT) occurs during embryogenesis or under pathological conditions such as hypoxia, injury, chronic inflammation, or tissue fibrosis. In renal tubular epithelial cells (MDCK), TGF-β1 induces EMT by reducing or increasing epithelial or mesenchymal marker expression, respectively. In this study, we confirmed that the cAMP analogues, 8-CPT-cAMP or N6-Ph-cAMP, inhibited the TGF-β1-driven overexpression of the mesenchymal markers ZEB-1, Slug, Fibronectin, and α-SMA. Furthermore, we showed that A1, A2A, P2Y1, P2Y11, and P2X7 purine receptor agonists modulated the TGF-β1-induced EMT through the involvement of PKA and/or MAPK/ERK signaling. The stimulation o…

0301 basic medicineMAPK/ERK pathwayMadin Darby canine kidney cellEpithelial-Mesenchymal TransitionFibrosiCellTransforming growth factor β1InflammationStimulationBiologyEpithelial to mesenchymal transition; Fibrosis; Madin Darby canine kidney cells; P1/P2 purinergic receptors; Transforming growth factor β1; Molecular Biology; Cellular and Molecular Neuroscience; Cell BiologyTransforming Growth Factor beta103 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineDogsmedicineAnimalsEpithelial–mesenchymal transitionReceptorMolecular BiologyEpithelial to mesenchymal transitionP1/P2 purinergic receptorReceptors Purinergic P2Mesenchymal stem cellReceptors Purinergic P1Cell BiologyMadin Darby canine kidney cellsFibrosisCell biologyFibronectin030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisbiology.proteinP1/P2 purinergic receptorsOriginal ArticleTransforming growth factor β1medicine.symptomTransforming growth factor
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ERK3/MAPK6 controls IL-8 production and chemotaxis

2020

ERK3 is a ubiquitously expressed member of the atypical mitogen activated protein kinases (MAPKs) and the physiological significance of its short half-life remains unclear. By employing gastrointestinal 3D organoids, we detect that ERK3 protein levels steadily decrease during epithelial differentiation. ERK3 is not required for 3D growth of human gastric epithelium. However, ERK3 is stabilized and activated in tumorigenic cells, but deteriorates over time in primary cells in response to lipopolysaccharide (LPS). ERK3 is necessary for production of several cellular factors including interleukin-8 (IL-8), in both, normal and tumorigenic cells. Particularly, ERK3 is critical for AP-1 signaling…

0301 basic medicineMAPK/ERK pathwayMouseQH301-705.5ScienceERK3General Biochemistry Genetics and Molecular BiologyCell Line03 medical and health sciencesMice0302 clinical medicineOrganoidmetastasisAnimalsHumansInterleukin 8Biology (General)chemotaxisMitogen-Activated Protein Kinase 6Gene knockdownGeneral Immunology and MicrobiologyIL-8ChemistryKinaseGeneral NeuroscienceQInterleukin-8RChemotaxisGeneral MedicineCell BiologyMAPKgastrointestinal organoidsIn vitroCell biologysecretomeChemotaxis Leukocyte030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisMedicineHeterograftsSignal transductionsignal transductionResearch ArticleHumaneLife
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A PTEN inhibitor displays preclinical activity against hepatocarcinoma cells

2016

Phosphatase and tensin homolog (PTEN) gene is considered a tumor suppressor gene. However, PTEN mutations rarely occur in hepatocellular carcinoma (HCC), whereas heterozygosity of PTEN, resulting in reduced PTEN expression, has been observed in 32–44% of HCC patients. In the present study, we investigated the effects of the small molecule PTEN inhibitor VO-OHpic in HCC cells. VO-OHpic inhibited cell viability, cell proliferation and colony formation, and induced senescence-associated β-galactosidase activity in Hep3B (low PTEN expression) and to a lesser extent in PLC/PRF/5 (high PTEN expression) cells, but not in PTEN-negative SNU475 cells. VO-OHpic synergistically inhibited cell viability…

0301 basic medicineMAPK/ERK pathwayPTENCarcinoma HepatocellularsenescenceTumor suppressor geneCell SurvivalMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineReportOrganometallic CompoundsAnimalsHumansPTENTensinViability assayHCCProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationbiologyCell growthTOR Serine-Threonine KinasesAKTLiver NeoplasmsPTEN PhosphohydrolaseCell BiologySorafenibXenograft Model Antitumor Assaysdigestive system diseasesVO-OHpicGene Expression Regulation Neoplastic030104 developmental biology030220 oncology & carcinogenesisbiology.proteinCancer researchSignal TransductionDevelopmental Biology
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Effects of mutations in Wnt/β-catenin, hedgehog, Notch and PI3K pathways on GSK-3 activity—Diverse effects on cell growth, metabolism and cancer

2016

Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase that participates in an array of critical cellular processes. GSK-3 was first characterized as an enzyme that phosphorylated and inactivated glycogen synthase. However, subsequent studies have revealed that this moon-lighting protein is involved in numerous signaling pathways that regulate not only metabolism but also have roles in: apoptosis, cell cycle progression, cell renewal, differentiation, embryogenesis, migration, regulation of gene transcription, stem cell biology and survival. In this review, we will discuss the roles that GSK-3 plays in various diseases as well as how this pivotal kinase interacts with multiple sign…

0301 basic medicineMAPK/ERK pathwaySettore MED/06 - Oncologia MedicaCellular differentiationPI3KTargeted therapyGlycogen Synthase Kinase 3Phosphatidylinositol 3-Kinases0302 clinical medicineGSK-3Neoplasmsbeta CateninGSK-3biologyReceptors NotchKinaseWnt signaling pathwayWnt/beta-cateninCell DifferentiationCell biologyGene Expression Regulation Neoplastic030220 oncology & carcinogenesismTORAkt; GSK-3; Hedgehog; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; mTORSignal TransductionBeta-cateninNotchAkt GSK-3 Hedgehog mTOR Notch PI3K Targeted therapy Therapy resistance Wnt/beta-cateninCell Survivalmacromolecular substancesNO03 medical and health sciencesAkt; GSK-3 Hedgehog Notch PI3K Targeted therapy Therapy resistance Wnt/beta-catenin mTORAnimalsHumansHedgehog ProteinsProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationAktTherapy resistanceAkt; GSK-3; Hedgehog; mTOR; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; Molecular Biology; Cell BiologyCell BiologyWnt ProteinsMicroRNAs030104 developmental biologyMutationCancer researchbiology.proteinTumor Suppressor Protein p53Hedgehog
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Targeting Angiogenesis in Biliary Tract Cancers: An Open Option

2017

Abstract: Biliary tract cancers (BTCs) are characterized by a bad prognosis and the armamentarium of drugs for their treatment is very poor. Although the inflammatory status of biliary tract represents the first step in the cancerogenesis, the microenvironment also plays a key role in the pathogenesis of BTCs, promoting tumor angiogenesis, invasion and metastasis. Several molecules, such as vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF), are involved in the angiogenesis process and their expression on tumor samples has been explored as prognostic marker in both cholangiocarcinoma and gallbladder cancer. Recent studies evaluated the genomic landscape of BTCs and…

0301 basic medicineMAPK/ERK pathwayVascular Endothelial Growth Factor AAngiogenesisDrug Evaluation PreclinicalTyrosine kinase inhibitorAngiogenesis InhibitorsReviewFibroblast growth factorCatalysiMetastasisAntineoplastic Agentlcsh:Chemistrychemistry.chemical_compoundangiogenesis0302 clinical medicinetyrosine kinase inhibitorsMolecular Targeted Therapylcsh:QH301-705.5SpectroscopyClinical Trials as TopicMonoclonal antibodieNeovascularization Pathologicvascular endothelial growth factorComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineComputer Science ApplicationsVascular endothelial growth factorGene Expression Regulation NeoplasticAngiogenesiChemistryBiliary Tract NeoplasmsTreatment OutcomeBiliary Tract Neoplasm030220 oncology & carcinogenesismonoclonal antibodiesTyrosine kinaseAngiogenesis InhibitorHumanSignal TransductionProtein Kinase InhibitorAntineoplastic Agentsbiliary tract cancersBiologyModels BiologicalAngiogenesis; Biliary tract cancers; Monoclonal antibodies; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Biliary Tract Neoplasms; Clinical Trials as Topic; Drug Evaluation Preclinical; Gene Expression Regulation Neoplastic; Genetic Variation; Humans; Models Biological; Neovascularization Pathologic; Protein Kinase Inhibitors; Signal Transduction; Treatment Outcome; Vascular Endothelial Growth Factor A; Molecular Targeted Therapy; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisInorganic Chemistry03 medical and health sciencesIn vivomedicineAnimalsHumansPhysical and Theoretical ChemistryGallbladder cancerMolecular BiologyProtein Kinase InhibitorsBiologyAnimalOrganic ChemistryGenetic Variationmedicine.disease030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Immunologyangiogenesis; biliary tract cancers; monoclonal antibodies; tyrosine kinase inhibitors; vascular endothelial growth factorCancer researchBiliary tract cancerInternational Journal of Molecular Sciences
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