Search results for " RNA interference"

showing 9 items of 9 documents

Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

2017

Abstract Thyroid carcinoma is generally associated with good prognosis, but no effective treatments are currently available for aggressive forms not cured by standard therapy. To find novel therapeutic targets for this tumor type, we had previously performed a siRNA-based functional screening to identify genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same extent for the viability of normal cells (non-oncogene addiction paradigm). Among those, we found the coatomer protein complex ζ1 (COPZ1) gene, which is involved in intracellular traffic, autophagy and lipid homeostasis. In this paper, we investigated the mechanisms through which COPZ…

0301 basic medicineCancer ResearchTime FactorsCOPZ1ApoptosisCOPZ1Thyroid cancerThyroid NeoplasmThyroidRNAi TherapeuticCell death; COPZ1; Non-oncogene addiction; Thyroid carcinoma; Animals; Apoptosis; Autophagy; Cell Line Tumor; Cell Survival; Coatomer Protein; Endoplasmic Reticulum Stress; Female; Gene Expression Regulation Neoplastic; Humans; Mice Nude; RNA Interference; Signal Transduction; Thyroid Neoplasms; Time Factors; Transfection; Tumor Burden; Unfolded Protein Response; Xenograft Model Antitumor Assays; RNAi Therapeutics; Oncology; Cancer ResearchEndoplasmic Reticulum StressOncogene AddictionTumor BurdenGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyFemaleRNA InterferenceNon-oncogene addictionHumanSignal TransductionCell deathProgrammed cell deathXenograft Model Antitumor AssayTime FactorCell SurvivalMice NudeBiologyTransfectionCoatomer ProteinThyroid carcinomaThyroid carcinoma03 medical and health sciencesCell Line TumorAutophagymedicineAnimalsHumansThyroid NeoplasmsEndoplasmic Reticulum StreAnimalAutophagyApoptosimedicine.diseaseXenograft Model Antitumor AssaysRNAi Therapeutics030104 developmental biologyImmunologyUnfolded Protein ResponseCancer researchUnfolded protein response
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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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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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Chemotherapy overcomes TRAIL-R4-mediated TRAIL resistance at the DISC level

2011

International audience; TNF-related apoptosis-inducing ligand or Apo2L (Apo2L/TRAIL) is a promising anti-cancer drug owing to its ability to trigger apoptosis by binding to TRAIL-R1 or TRAIL-R2, two membrane-bound receptors that are often expressed by tumor cells. TRAIL can also bind non-functional receptors such as TRAIL-R4, but controversies still exist regarding their potential to inhibit TRAIL-induced apoptosis. We show here that TRAIL-R4, expressed either endogenously or ectopically, inhibits TRAIL-induced apoptosis. Interestingly, the combination of chemotherapeutic drugs with TRAIL restores tumor cell sensitivity to apoptosis in TRAIL-R4-expressing cells. This sensitization, which ma…

MESH: CASP8 and FADD-Like Apoptosis Regulating ProteinMESH : Antineoplastic Combined Chemotherapy ProtocolsCASP8 and FADD-Like Apoptosis Regulating ProteinTRAILApoptosisMESH : Models BiologicalMitochondrionMESH : RNA Small InterferingMESH: Caspase 8TNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandMESH : Tumor Necrosis Factor Decoy Receptors0302 clinical medicineRNA interferenceNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsMESH: RNA Small InterferingMESH: NeoplasmsRNA Small InterferingReceptorSensitizationCaspase 80303 health sciencesMESH : Caspase 8MESH: Drug Resistance Neoplasm3. Good healthCell biologyMESH: Antineoplastic Combined Chemotherapy ProtocolsMESH : Drug Resistance Neoplasmmedicine.anatomical_structure030220 oncology & carcinogenesisRNA InterferenceMESH : GPI-Linked ProteinsMESH: TNF-Related Apoptosis-Inducing LigandDeath Domain Receptor Signaling Adaptor ProteinsProgrammed cell deathMESH: Cell Line Tumorc-FLIPMESH: RNA InterferenceBiologyGPI-Linked ProteinsCaspase 8Models Biological03 medical and health sciencesCell Line TumorReceptors Tumor Necrosis Factor Member 10cmedicineTRAIL-R4HumanscancerChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology030304 developmental biologyOriginal PaperMESH: HumansMESH : Cell Line TumorMESH: ApoptosisMESH : HumansMESH: Models BiologicalMESH : CASP8 and FADD-Like Apoptosis Regulating ProteinCell BiologyMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : NeoplasmsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsDrug Resistance NeoplasmApoptosisMESH : RNA InterferenceMESH: GPI-Linked ProteinsMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsMESH: Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy Receptors
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p14(ARF) Prevents Proliferation of Aneuploid Cells by Inducing p53-Dependent Apoptosis.

2014

Weakening the Spindle Assembly Checkpoint by reduced expression of its components induces chromosome instability and aneuploidy that are hallmarks of cancer cells. The tumor suppressor p14(ARF) is overexpressed in response to oncogenic stimuli to stabilize p53 halting cell progression. Previously, we found that lack or reduced expression of p14(ARF) is involved in the maintenance of aneuploid cells in primary human cells, suggesting that it could be part of a pathway controlling their proliferation. To investigate this aspect further, p14(ARF) was ectopically expressed in HCT116 cells after depletion of the Spindle Assembly Checkpoint MAD2 protein that was used as a trigger for aneuploidy. …

Mad2 ProteinApoptosis; M Phase Cell Cycle Checkpoints; Mad2 Proteins; RNA Interference; Tumor Suppressor Protein p14ARF; AneuploidyApoptosiMitosisApoptosisM Phase Cell Cycle CheckpointAneuploidyHCT116 CellsSettore BIO/18 - GeneticaGene Knockout TechniquesMad2 ProteinsTumor Suppressor Protein p14ARFHumansM Phase Cell Cycle CheckpointsRNA InterferenceTumor Suppressor Protein p53Cell ProliferationJournal of cellular physiology
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Transport of the major myelin proteolipid protein is directed by VAMP3 and VAMP7.

2011

CNS myelination by oligodendrocytes requires directed transport of myelin membrane components and a timely and spatially controlled membrane expansion. In this study, we show the functional involvement of the R-solubleN-ethylmaleimide-sensitive factor attachment protein receptor (R-SNARE) proteins VAMP3/cellubrevin and VAMP7/TI-VAMP in myelin membrane trafficking. VAMP3 and VAMP7 colocalize with the major myelin proteolipid protein (PLP) in recycling endosomes and late endosomes/lysosomes, respectively. Interference with VAMP3 or VAMP7 function using small interfering RNA-mediated silencing and exogenous expression of dominant-negative proteins diminished transport of PLP to the oligodendro…

MaleProteolipid protein 1Vesicle-Associated Membrane Protein 3MESH: Myelin SheathMESH: R-SNARE Proteins[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyR-SNARE ProteinsMiceMyelin0302 clinical medicineMESH: Microscopy ImmunoelectronMESH: Genetic VectorsImage Processing Computer-AssistedMESH: AnimalsMicroscopy ImmunoelectronMESH: Myelin Proteolipid ProteinCells CulturedMyelin SheathMESH: Vesicle-Associated Membrane Protein 3VAMP30303 health sciencesMESH: ExocytosisGeneral NeuroscienceMESH: Enzyme-Linked Immunosorbent AssayArticlesImmunohistochemistryMESH: Image Processing Computer-AssistedMyelin proteolipid proteinCell biologymedicine.anatomical_structureElectrophoresis Polyacrylamide GelFemaleRNA InterferenceMESH: Cells CulturedEndosomeGenetic VectorsMESH: RNA InterferenceBiological Transport ActiveEnzyme-Linked Immunosorbent AssayEndosomesBiologyTransfectionExocytosisExocytosis03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsSecretionMyelin Proteolipid ProteinMESH: MiceSecretory pathway030304 developmental biologyMESH: TransfectionCell MembraneMESH: ImmunohistochemistryMESH: MaleMice Inbred C57BLnervous systemMESH: EndosomesMESH: Biological Transport ActiveLysosomesMESH: Female030217 neurology & neurosurgeryMESH: LysosomesMESH: Cell MembraneMESH: Electrophoresis Polyacrylamide Gel
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Expression of T-cadherin in tumor cells influences invasive potential of human hepatocellular carcinoma

2006

Overexpression of T-cadherin (T-cad) transcripts occurs in approximately 50% of human hepatocellular carcinomas (HCCs). To elucidate T-cad functions in HCC, we examined T-cad protein expression in normal and tumoral human livers and hepatoma cell lines and investigated its influence on invasive potential of HCC using RNA interference silencing of T-cad expression in Mahlavu cells. Whereas T-cad expression was restricted to endothelial cells (EC) from large blood vessels in normal livers, it was up-regulated in sinusoidal EC from 8/15 invasive HCCs. Importantly, in three of them (38%) T-cad was detected in tumor cells within regions in which E-cadherin expression was absent. Among six hepato…

Pathologymedicine.medical_specialtyCarcinoma HepatocellularTranscription GeneticLiver cytologyCell Culture TechniquesMotilityBiologyTransfectionBiochemistryRNA interferenceCell MovementCell Line TumorGeneticsmedicineGene silencingAnimalsHumansNeoplasm Invasivenesscardiovascular diseasesRNA Small InterferingMolecular BiologyDNA PrimersWound Healingprimary tumors cadherin switch cell invasion hepatoma cell lines RNA interferenceLiver NeoplasmsEndothelial CellsTransfectionHCCSFibroblastsCadherinsdigestive system diseasesT-cadherinLiverCell cultureCancer researchHepatocytesRabbitsCell DivisionBiotechnology
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RNA memory model: a RNA-mediated transcriptional activation mechanism involved in cell identity.

2010

Position-effect variegation (PEV) was discovered in Drosophila melanogaster in 1930 in a study of X-ray-induced chromosomal rearrangements. If a rearrangement places euchromatic genes adjacent to a region of centromeric heterochromatin, it gives a variegated phenotype that results from the random inactivation of genes by heterochromatin spreading from the breakpoint. After the establishment, the inactivation is henceforth clonally inherited. The vast majority of these modifiers were originally isolated in Drosophila as dominant mutations that suppressed or enhanced the variegation caused by a variegating white allele called white-mottled 4 (wm4). A large number of modifier genes alter PEV p…

Transcriptional ActivationAgingBiologyModels BiologicalCell Physiological PhenomenaDNA-directed RNA interferenceRNA interferenceTranscription (biology)AnimalsHumansGene SilencingSmall nucleolar RNAGeneticsPEV RNA Transinduction Cell Identity TransdifferentiationNucleic Acid HeteroduplexesRNACell DifferentiationNon-coding RNALong non-coding RNAChromatinRNA silencingDrosophila melanogasterRNARNA InterferenceGeriatrics and Gerontologyrna memory memRNA epigeneticsRejuvenation research
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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