Search results for " Neoplastic"

showing 10 items of 662 documents

SCD5-induced oleic acid production reduces melanoma malignancy by intracellular retention of SPARC and cathepsin B

2014

A proper balance between saturated and unsaturated fatty acids (FAs) is required for maintaining cell homeostasis. The increased demand of FAs to assemble the plasma membranes of continuously dividing cancer cells might unbalance this ratio and critically affect tumour outgrowth. We unveiled the role of the stearoyl-CoA desaturase SCD5 in converting saturated FAs into mono-unsaturated FAs during melanoma progression. SCD5 is down-regulated in advanced melanoma and its restored expression significantly reduced melanoma malignancy, both in vitro and in vivo, through a mechanism governing the secretion of extracellular matrix proteins, such as secreted protein acidic and rich in cysteine (SPAR…

cathepsin B2734Intracellular SpaceDown-RegulationCell LineMelanocyteCell Line TumormelanomaHumansintracellular acidityOsteonectinNeoplasticTumorMedicine (all)Fatty AcidsSPARCHydrogen-Ion ConcentrationGene Expression Regulation NeoplasticSCD5Gene Expression Regulationoleic acidDisease ProgressionMelanocytesFatty AcidStearoyl-CoA Desaturasecathepsin B; intracellular acidity; melanoma; oleic acid; SCD5; SPARC; Cathepsin B; Cell Line Tumor; Disease Progression; Down-Regulation; Fatty Acids; Humans; Hydrogen-Ion Concentration; Intracellular Space; Melanocytes; Melanoma; Oleic Acid; Osteonectin; Stearoyl-CoA Desaturase; Gene Expression Regulation Neoplastic; 2734; Medicine (all)Human
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The Status of EGFR Modulates the Effect of miRNA-200c on ZEB1 Expression and Cell Migration in Glioblastoma Cells

2020

Migration of glioblastoma cells into surrounding tissue is one of the main features that makes this tumor incurable. We evaluated whole-genome miRNA expression profiling associated with different EGFR amplification patterns in 30 cases of primary glioblastoma. From the 64 miRNAs that showed differential expression between tumors with a high level of EGFR amplification and tumors without EGFR amplification, 40% were related with cell migration, being miR-200c the most differentially expressed between these two groups. We investigated the effect of miR-200c on ZEB1 expression and cell migration in an in vitro transfection model with a miR-200c mimic, a miR-200c inhibitor and siRNA targeting E…

cell migrationEGFR AmplificationApoptosisBiologyArticleCatalysismiR-200clcsh:ChemistryInorganic ChemistryDownregulation and upregulationCell MovementmicroRNABiomarkers TumorTumor Cells CulturedmedicineZEB1HumansGene silencingEGFR amplificationPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyCell ProliferationOrganic ChemistryglioblastomaGene AmplificationZinc Finger E-box-Binding Homeobox 1Cell migrationGeneral MedicineTransfectionPrognosismedicine.diseaseComputer Science ApplicationsErbB ReceptorsGene Expression Regulation NeoplasticMicroRNAslcsh:Biology (General)lcsh:QD1-999Cell cultureMutationCancer researchGlioblastomaInternational Journal of Molecular Sciences
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Bleomycin: Action on growth of oncogenic RNA viruses and on cell transformation

1975

Bleomycin (BLM) inhibits cell proliferation of noninfected chick embryo fibroblasts by blocking their DNA synthesis selectively. Chick embryo fibroblasts have beentransformed by Schmidt-Ruppin D strain of Rous Sarcoma Virus. Transformation has been determined by a focus assay. Foci formation is strongly reduced by BLM. Virus replication is inhibited by BLM in growing and confluent monolayer cells. This result might be explained by the observation that this drug reduces proliferation of growing and of confluent monolayer cells very sensitively. During the first 24 hours after infection the BLM inhibitory effect is more pronounced than in the case of BLM-application during the period 24--48 h…

congenital hereditary and neonatal diseases and abnormalitiesTime Factorsanimal structuresTranscription GeneticCell divisionCellChick EmbryoBiologyVirus ReplicationVirusBleomycinTranscription (biology)VirologymedicineAnimalsRNA VirusesCells CulturedRous sarcoma virusurogenital systemCell growthnutritional and metabolic diseasesRNADNAGeneral MedicineFibroblastsbiology.organism_classificationVirologyMolecular biologyCell Transformation Neoplasticmedicine.anatomical_structureAvian Sarcoma VirusesViral replicationembryonic structuresRNARNA ViralArchives of Virology
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Annexin-1 downregulation in thyroid cancer correlates to the degree of tumour differentiation

2006

We investigated the expression of annexin-1 (ANXA1) in thyroid carcinoma cell lines and in thyroid cancers with a different degree of differentiation. The highest level of ANXA1 expression examined by Western blotting was detected in the papillary carcinoma cells (NPA) and in the follicular cells (WRO). On the other hand, the most undifferentiated thyroid carcinoma cells (ARO and FRO) presented the lowest level of ANXA1 expression. In surgical tissue specimens from 32 patients with thyroid cancers, we found high immunoreactivity for ANXA1 in papillary (PTC) and follicular (FTC) thyroid cancers while in undifferentiated thyroid cancers (UTC) the expression of the protein was barely detectabl…

endocrine systemCancer ResearchPathologymedicine.medical_specialtyannexin-1endocrine system diseasesCellular differentiationThyroid Glandmedicine.disease_causeThyroid carcinomaDownregulation and upregulationannexinopathieTumor Cells CulturedmedicineHumansThyroid Neoplasmsdifferentiation markerThyroid cancerThyroid NeoplasmAnnexin A1PharmacologyRegulation of gene expressionbusiness.industryThyroidCell Differentiationmedicine.diseaseapoptosithyroid carcinomaGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyCell cultureMolecular MedicineCarcinogenesisbusinessHumanCancer Biology & Therapy
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RASSF1A inhibits estrogen receptor alpha expression and estrogen-independent signalling: implications for breast cancer development

2012

The Ras association domain family 1 isoform A (RASSF1A) is a tumor suppressor whose inactivation is implicated in the development of many human cancers, including breast carcinomas. Little is known about the tumor-suppressive function of RASSF1A in breast tissue and whether its inactivation is mechanistically involved in the initiation and progression of breast tumors. Here, we show that RASSF1A inhibits breast cancer growth in vivo, and suppresses estrogen receptor (ERα) expression and function. Reconstitution of RASSF1A in MCF7 cells led to decreased ERα levels and reduced sensitivity to estrogen (E2). Concomitantly, we observed decreased expression of Id1 as well as the E2-responsive gen…

endocrine systemCancer Researchmedicine.medical_specialtyCell SurvivalGene ExpressionEstrogen receptorApoptosisBreast NeoplasmsCell Cycle ProteinsMice SCIDBiologyMiceBreast cancerDownregulation and upregulationMice Inbred NODInternal medicineGeneticsmedicineAnimalsHumansFulvestrantMolecular BiologyCellular SenescenceCell ProliferationRegulation of gene expressionEstradiolFulvestrantTumor Suppressor ProteinsEstrogen AntagonistsEstrogen Receptor alphaCancerEstrogensCell Cycle Checkpointsmedicine.diseaseGene Expression Regulation NeoplasticEndocrinologyProteolysisMCF-7 CellsCancer researchFemaleEctopic expressionEstrogen receptor alphaNeoplasm TransplantationSignal Transductionmedicine.drugOncogene
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The NG2 Proteoglycan Protects Oligodendrocyte Precursor Cells against Oxidative Stress via Interaction with OMI/HtrA2.

2015

The NG2 proteoglycan is characteristically expressed by oligodendrocyte progenitor cells (OPC) and also by aggressive brain tumours highly resistant to chemo- and radiation therapy. Oligodendrocyte-lineage cells are particularly sensitive to stress resulting in cell death in white matter after hypoxic or ischemic insults of premature infants and destruction of OPC in some types of Multiple Sclerosis lesions. Here we show that the NG2 proteoglycan binds OMI/HtrA2, a mitochondrial serine protease which is released from damaged mitochondria into the cytosol in response to stress. In the cytosol, OMI/HtrA2 initiates apoptosis by proteolytic degradation of anti-apoptotic factors. OPC in which NG…

lcsh:MedicineApoptosisdrug effects [Cytosol]HTRA2 protein humangenetics [RNA Small Interfering]genetics [Serine Endopeptidases]genetics [Glioblastoma]570 Life sciencespathology [Glioblastoma]MiceCytosolCerebellumpathology [Cerebellum]RNA Small Interferinglcsh:Sciencemetabolism [Antigens]Mice Knockoutchondroitin sulfate proteoglycan 4metabolism [Proteoglycans]Brain NeoplasmsSerine Endopeptidasesdrug effects [Mitochondria]metabolism [Cerebellum]High-Temperature Requirement A Serine Peptidase 2Mitochondriametabolism [Brain Neoplasms]Gene Expression Regulation Neoplasticpharmacology [Antibodies Neutralizing]genetics [Mitochondrial Proteins]Proteoglycans570 BiowissenschaftenResearch ArticleProtein BindingSignal Transductionpathology [Brain Neoplasms]Primary Cell Culturedrug effects [Cerebellum]drug effects [Apoptosis]metabolism [Mitochondrial Proteins]Mitochondrial Proteinsantagonists & inhibitors [Proteoglycans]pharmacology [Hydrogen Peroxide]genetics [Antigens]Cell Line Tumormetabolism [Serine Endopeptidases]AnimalsHumansddc:610metabolism [RNA Small Interfering]Antigenslcsh:RHtra2 protein mouseHydrogen Peroxidemetabolism [Mitochondria]Antibodies Neutralizinggenetics [Proteoglycans]genetics [Brain Neoplasms]Mice Inbred C57BLOxidative Stressnervous systemlcsh:Qmetabolism [Cytosol]Glioblastomametabolism [Glioblastoma]
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EGF-Induced Acetylation of Heterogeneous Nuclear Ribonucleoproteins Is Dependent on KRAS Mutational Status in Colorectal Cancer Cells.

2015

KRAS mutational status is considered a negative predictive marker of the response to anti-EGFR therapies in colorectal cancer (CRC) patients. However, conflicting data exist regarding the variable response to EGFR-targeted therapy. The effects of oncogenic KRAS on downstream targets were studied in cell lines with different KRAS mutations. Cells harboring a single KRASG13D allele showed the most tumorigenic profile, with constitutive activation of the downstream pathway, rendering them EGF-unresponsive. Conversely, KRASA146T cells showed a full EGF-response in terms of signal transduction pathways, cell proliferation, migration or adhesion. Moreover, the global acetylome of CRC cells was al…

lcsh:MedicineBiologymedicine.disease_causeHeterogeneous-Nuclear RibonucleoproteinsProto-Oncogene Proteins p21(ras)Epidermal growth factorCell Line TumormedicineHumansCell adhesionlcsh:ScienceMutationMultidisciplinaryEpidermal Growth FactorCell growthlcsh:RAcetylationCell migrationHCT116 CellsGene Expression Regulation NeoplasticDrug Resistance NeoplasmAcetylationMutationCancer researchlcsh:QKRASSignal transductionColorectal NeoplasmsResearch ArticleSignal TransductionPLoS ONE
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Mutant HRAS as novel target for MEK and mTOR inhibitors.

2015

HRAS is a frequently mutated oncogene in cancer. However, mutant HRAS as drug target has not been investigated so far. Here, we show that mutant HRAS hyperactivates the RAS and the mTOR pathway in various cancer cell lines including lung, bladder and esophageal cancer. HRAS mutation sensitized toward growth inhibition by the MEK inhibitors AZD6244, MEK162 and PD0325901. Further, we found that MEK inhibitors induce apoptosis in mutant HRAS cell lines but not in cell lines lacking RAS mutations. In addition, knockdown of HRAS by siRNA blocked cell growth in mutant HRAS cell lines. Inhibition of the PI3K pathway alone or in combination with MEK inhibitors did not alter signaling nor had an imp…

mTOR inhibitorMutantBlotting Western610 Medicine & healthApoptosisMice SCIDCell LineProto-Oncogene Proteins p21(ras)chemistry.chemical_compoundCell Line TumorNeoplasmsMedicineAnimalsHumansHRASHRAS mutationsProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationGeneticsMitogen-Activated Protein Kinase KinasesMEK inhibitorOncogeneCell growthbusiness.industryMEK inhibitorTOR Serine-Threonine KinasesDiphenylamineXenograft Model Antitumor AssaysTumor Burdenlung cancer10219 Clinic for Gastroenterology and HepatologyCell Transformation NeoplasticOncologychemistry10032 Clinic for Oncology and HematologyBenzamidesMutationCancer researchbladder cancer2730 OncologyBenzimidazolesRNA InterferenceSignal transductionGrowth inhibitionbusinessSignal TransductionResearch PaperOncotarget
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Carcinogenic aspect of xenobiotic molecules belonging to the peroxisome proliferator family.

1999

It is known that a short-term exposure of rat, mice or incubation of hepatic cells with fibrate molecules leads to increase in peroxisome number and cell hyperplasia. Further, long-term incubation of cells (at least a year) show transformed characteristics with foci and nodules. To explain the hepatocarcinogenic effect of peroxisome proliferators in rodents we studied the effect of peroxisome proliferators on rat liver oncogenes expression. Earlier, we reported an increase in liver and kidney mRNA level of c-myc and N-myc. Since several metabolic genes are activated by PPAR (peroxisome proliferators activated receptor) through a PPRE (peroxisome proliferator response element), we suggest th…

medicine.drug_classCarcinogenicity TestsResponse elementGuinea PigsPeroxisome proliferator-activated receptorPeroxisome ProliferationRodentiaFibrateBiologyXenobioticsGeneticsmedicineTumor Cells CulturedAnimalsHumansReceptorchemistry.chemical_classificationGeneral MedicineOncogenesPeroxisomeMolecular biologyCell biologyRatsCell Transformation NeoplasticchemistryHepatic stellate cellCarcinogensPeroxisome ProliferatorsCiprofibrateCell Divisionmedicine.drugHepatomegalyInternational journal of molecular medicine
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Geranylgeranyl as well as farnesyl moiety is transferred to Ras p21 overproduced in adrenocortical cells transformed by c-Ha-rasEJ oncogene.

1997

The ras-transformed newborn rat adrenocortical (RTAC) cells were obtained by transfection with the mutated c-Ha-rasEJ oncogene. They are proliferative and tumorigenic cells characterized by expression of the c-Ha-rasEJ oncogene and overexpression of a wild-type ras oncogene. The overproduced Ras p21 was identified here as Ki-Ras p21 by western blotting using a specific anti-Ki-Ras monoclonal antibody. Radioactivity derived from [14C]mevalonolactone was strongly incorporated into Ras p21 overproduced in RTAC cells. RTAC cells pretreated with lovastatin and labeled with either [3H]geranylgeranyl-pyrophosphate or [3H]farnesyl-pyrophosphate incorporated also radioactivity into Ras p21. These re…

medicine.drug_classChemistryBiophysicsProtein PrenylationMevalonic AcidCell BiologyTransfectionMonoclonal antibodyBiochemistryMolecular biologyRatsBlotProto-Oncogene Proteins p21(ras)GeranylgeranylationCell Transformation NeoplasticPrenylationmedicineAdrenal CortexMoietyAnimalsLovastatinMolecular Biologymedicine.drugBiochemical and biophysical research communications
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