Search results for " Neoplastic"

showing 10 items of 662 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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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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PTEN status is a crucial determinant of the functional outcome of combined MEK and mTOR inhibition in cancer

2017

AbstractCombined MAPK/PI3K pathway inhibition represents an attractive, albeit toxic, therapeutic strategy in oncology. Since PTEN lies at the intersection of these two pathways, we investigated whether PTEN status determines the functional response to combined pathway inhibition. PTEN (gene, mRNA, and protein) status was extensively characterized in a panel of cancer cell lines and combined MEK/mTOR inhibition displayed highly synergistic pharmacologic interactions almost exclusively in PTEN-loss models. Genetic manipulation of PTEN status confirmed a mechanistic role for PTEN in determining the functional outcome of combined pathway blockade. Proteomic analysis showed greater phosphoprote…

0301 basic medicineMAPK/ERK pathwayPTENRNA interferenceprotein Kinase inhibitorsRNA Small InterferinghumansPhosphoinositide-3 Kinase InhibitorsAnimals; cell line tumor; drug synergism; everolimus; female; humans; Janus Kinase 1; MAP Kinase Kinase Kinases; mice; neoplastic stem cells; PTEN phosphohydrolase; phosphatidylinositol 3-Kinases; protein Kinase inhibitors; proto-oncogene Proteins c-akt; Pyridones; Pyrimidinones; RNA Interference; RNA Small Interfering; STAT3 Transcription Factor; TOR Serine-Threonine KinasesMultidisciplinaryMAPK/PI3K pathway inhibitiononcology MAPK/PI3K pathway inhibitionTOR Serine-Threonine Kinasescell lineMAPK/PI3K inhibition oncology. inhibition. PTEN gene mRNA cancer cell lines MEK/mTORMAP Kinase Kinase KinasesfemaleoncologymTORRNA InterferenceSTAT3 Transcription FactortumormicePyridonesMice NudePyrimidinonesBiologyphosphatidylinositol 3-KinasesSmall InterferingArticle03 medical and health sciencesMediatorSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicinePTENAnimalsPI3K/AKT/mTOR pathwaydrug synergismSettore MED/06 - ONCOLOGIA MEDICAneoplastic stem cellsRPTORCancerJanus Kinase 1medicine.diseaseeverolimusproto-oncogene Proteins c-aktBlockade030104 developmental biologyCancer researchbiology.proteinRNAPTEN phosphohydrolase
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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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DNA methylomes reveal biological networks involved in human eye development, functions and associated disorders

2017

This work provides a comprehensive CpG methylation landscape of the different layers of the human eye that unveils the gene networks associated with their biological functions and how these are disrupted in common visual disorders. Herein, we firstly determined the role of CpG methylation in the regulation of ocular tissue-specification and described hypermethylation of retinal transcription factors (i.e., PAX6, RAX, SIX6) in a tissue-dependent manner. Second, we have characterized the DNA methylome of visual disorders linked to internal and external environmental factors. Main conclusions allow certifying that crucial pathways related to Wnt-MAPK signaling pathways or neuroinflammation are…

0301 basic medicineMaleADNlcsh:MedicineUllRetinal NeovascularizationEyeEpigenesis Genetic0302 clinical medicinelcsh:ScienceChildCàncerCancerRegulation of gene expressionMultidisciplinaryRetinoblastomaMelanomaMethylationDNA NeoplasmOphthalmopathiesNeoplasm ProteinsGene Expression Regulation NeoplasticOftalmologiaChild PreschoolDNA methylationFemaleMetilacióOftalmopatiesAdultMAP Kinase Signaling SystemBiologyMethylationArticle03 medical and health sciencesETS1medicineHumansEye ProteinsTranscription factorDiabetic RetinopathyEye Neoplasmslcsh:RDNADNA Methylationmedicine.diseaseeye diseasesOphthalmology030104 developmental biologyImmunology030221 ophthalmology & optometryCancer researchlcsh:QPAX6
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Peroxisome proliferator-activated receptor alpha deficiency impairs regulatory T cell functions: Possible application in the inhibition of melanoma t…

2016

International audience; Regulatory T (Treg) cells are important to induce and maintain immunological self-tolerance. Although the progress accomplished in understanding the functional mechanism of Treg cells, intracellular molecules that control the mechanisms of their suppressive capacity are still on investigation. The present study showed that peroxisome proliferator-activated receptor-alpha deficiency impaired the suppressive activity of Treg cells on CD4(+)CD25(-) and CD8(+) T cell proliferation. In Treg cells, PPARα gene deletion also induced a decrease of migratory abilities, and downregulated the expression of chemokine receptors (CCR-4, CCR-8 and CXCR-4) and p27(KIP1) mRNA. Treg ce…

0301 basic medicineMaleAdoptive cell transferMESH: Tumor BurdenB16 melanoma tumorMelanoma ExperimentalMESH: T-Lymphocyte SubsetsCD4(+)CD25(+) regulatory T cellsBiochemistryMESH: Mice KnockoutImmunotherapy AdoptiveT-Lymphocytes RegulatoryPPARαMESH : T-Lymphocytes RegulatoryCell MovementT-Lymphocyte SubsetsMESH: Reverse Transcriptase Polymerase Chain ReactionMESH : Cell ProliferationMESH : Cell MovementMESH: AnimalsIL-2 receptorMESH: PPAR alphaMESH: Cell MovementCells CulturedMice KnockoutMESH : Melanoma ExperimentalbiologyMESH : Tumor BurdenReverse Transcriptase Polymerase Chain ReactionMESH : Reverse Transcriptase Polymerase Chain ReactionFOXP3hemic and immune systemsGeneral MedicineMESH: Gene Expression Regulation Neoplastic3. Good healthTumor BurdenMESH: Melanoma ExperimentalDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureMESH: Immunotherapy AdoptiveReceptors ChemokineMESH : DNA-Binding ProteinsMESH: Cells Culturedmedicine.medical_specialtyMESH : Receptors ChemokineMESH: Cell Line TumorRegulatory T cellMESH : Gene Expression Regulation NeoplasticT cellMESH : MaleMESH : PPAR alphachemical and pharmacologic phenomenaMESH : Mice Inbred C57BLMESH : Clonal Anergy03 medical and health sciencesMESH: Mice Inbred C57BLInternal medicineMESH: Cell ProliferationCell Line TumorMESH : Cells CulturedmedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPPAR alpha[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCell ProliferationClonal AnergyPerforinMESH : Cell Line TumorMESH: T-Lymphocytes RegulatoryMolecular biologyMESH: MaleMESH : T-Lymphocyte SubsetsGranzyme BMice Inbred C57BL030104 developmental biologyEndocrinologyPerforinMESH: Clonal Anergybiology.proteinMESH : Mice KnockoutMESH : AnimalsMESH: Receptors ChemokineCD8MESH: DNA-Binding ProteinsMESH : Immunotherapy Adoptive
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miR-21 antagonism abrogates Th17 tumor promoting functions in multiple myeloma

2020

Multiple myeloma (MM) is tightly dependent on inflammatory bone marrow microenvironment. IL-17 producing CD4+ T cells (Th17) sustain MM cells growth and osteoclasts-dependent bone damage. In turn, Th17 differentiation relies on inflammatory stimuli. Here, we investigated the role of miR-21 in Th17-mediated MM tumor growth and bone disease. We found that early inhibition of miR-21 in naive T cells (miR-21i-T cells) impaired Th17 differentiation in vitro and abrogated Th17-mediated MM cell proliferation and osteoclasts activity. We validated these findings in NOD/SCID-g-NULL mice, intratibially injected with miR-21i-T cells and MM cells. A Pairwise RNAseq and proteome/phosphoproteome analysis…

0301 basic medicineMaleCancer ResearchBone diseaseApoptosisBone NeoplasmsNodMice SCIDBone NeoplasmT-Lymphocytes RegulatoryTh17 Cell03 medical and health sciencesMice0302 clinical medicineDownregulation and upregulationgammopathiesMice Inbred NODmedicineTumor Cells CulturedTumor MicroenvironmentBiomarkers TumorAnimalsHumansMultiple myelomaCell ProliferationChemistryCell growthAnimalApoptosiHematologymedicine.diseasePrognosisXenograft Model Antitumor AssaysIn vitroGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCase-Control StudiesCancer researchTh17 CellsBone marrowAntagonismCase-Control StudieMultiple Myeloma
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