Search results for "Downregulation"

showing 10 items of 460 documents

Downregulation of RhoB GTPase confers resistance to cisplatin in human larygneal carcinoma cells

2009

Acquired resistance to cisplatin represents a major obstacle to an efficient chemotherapy. We found downregulation of RhoB expression in cisplatin-resistant tumor cell lines from different origin. In cisplatin-resistant laryngeal carcinoma subline overexpression of farnesylated or geranylgeranylated RhoB increased cisplatin-induced cell death, while silencing of RhoB expression diminished sensitivity of parental HEp-2 cells via decreased cellular accumulation of cisplatin. However, since RhoB silencing in additional tumor cell lines did not alter their sensitivity to cisplatin, we can assume that RhoB downregulation does not provide general protective role in cell response to cisplatin. Nev…

Cancer ResearchProgrammed cell deathGenetic enhancementRHOBmedicine.medical_treatmentDown-RegulationAntineoplastic AgentsBiologyDownregulation and upregulationCell Line TumormedicineCarcinomaHumansGene silencingrhoB GTP-Binding ProteinLaryngeal NeoplasmsCisplatinChemotherapymedicine.diseaseCell biologyOncologyDrug Resistance NeoplasmCancer researchcisplatin ; drug resistance ; Rho GTPases ; RhoBCisplatinmedicine.drug
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Pleiotropic antitumor effects of the pan-HDAC inhibitor ITF2357 against c-Myc-overexpressing human B-cell non-Hodgkin lymphomas

2014

Histone deacetylases (HDAC) extensively contribute to the c-Myc oncogenic program, pointing to their inhibition as an effective strategy against c-Myc-overexpressing cancers. We, thus, studied the therapeutic activity of the new-generation pan-HDAC inhibitor ITF2357 (Givinostat®) against c-Myc-overexpressing human B-cell non-Hodgkin lymphomas (B-NHLs). ITF2357 anti-proliferative and pro-apoptotic effects were analyzed in B-NHL cell lines with c-Myc translocations (Namalwa, Raji and DOHH-2), stabilizing mutations (Raji) or post-transcriptional alterations (SU-DHL-4) in relationship to c-Myc modulation. ITF2357 significantly delayed the in vitro growth of all B-NHL cell lines by inducing G1 c…

Cancer ResearchProgrammed cell deathOncologyDownregulation and upregulationCell cultureIn vivohemic and lymphatic diseasesmicroRNACancer researchBiologyReceptorProtein kinase BPI3K/AKT/mTOR pathwayInternational Journal of Cancer
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ERBB2 Induces an Antiapoptotic Expression Pattern of Bcl-2 Family Members in Node-Negative Breast Cancer

2010

AbstractPurpose: Members of the Bcl-2 family act as master regulators of mitochondrial homeostasis and apoptosis. We analyzed whether ERBB2 influences the prognosis of breast cancer by influencing the proapoptotic versus antiapoptotic balance of Bcl-2 family members.Experimental Design: ERBB2-regulated Bcl-2 family members were identified by inducible expression of ERBB2 in MCF-7 breast cancer cells and by correlation analysis with ERBB2 expression in breast carcinomas. The prognostic relevance of ERBB2-regulated and all additional Bcl-2 family members was determined in 782 patients with untreated node-negative breast cancer. The biological relevance of ERBB2-induced inhibition of apoptosis…

Cancer ResearchReceptor ErbB-2Transplantation HeterologousMedizinApoptosisBreast NeoplasmsBiologyBioinformaticsModels BiologicalBAG1Cohort StudiesMiceBreast cancerDownregulation and upregulationTumor Cells CulturedmedicineAnimalsHumansskin and connective tissue diseasesOligonucleotide Array Sequence AnalysisClusterinGene Expression ProfilingCarcinomaBcl-2 familyCancermedicine.diseaseGenes bcl-2Gene Expression Regulation NeoplasticTransplantationOncologyMultigene FamilyBCL2L13NIH 3T3 CellsCancer researchbiology.proteinFemaleLymph NodesApoptosis Regulatory ProteinsClinical Cancer Research
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Interleukin-6 and the soluble interleukin-6 receptor induce stem cell factor and Flt-3L expression in vivo and in vitro.

2001

Abstract Objective We recently established transgenic animals expressing either interleukin-6 (IL-6) or the soluble IL-6 receptor (sIL-6R) alone, or both components, IL-6 and the sIL-6R, in the liver. This animal model demonstrated that the expression of IL-6 in combination with its sIL-6R led to extramedullary expansion of hematopoietic progenitor cells in the spleen and liver. Materials and Methods We studied other relevant hematopoietic cytokines involved in the IL-6/sIL-6R–induced stimulation of hematopoiesis. Results Using immunohistochemistry, we showed that cell-associated stem cell factor (SCF) and Flt-3L expression were upregulated in liver and spleen only in double transgenic mice…

Cancer ResearchStromal cellCD34Fluorescent Antibody TechniqueStem cell factorMice TransgenicMiceDownregulation and upregulationIn vivoGeneticsAnimalsHumansRNA MessengerReceptorInterleukin 6Molecular BiologyImmunosorbent TechniquesStem Cell FactorbiologyInterleukin-6Membrane ProteinsCell BiologyHematology3T3 CellsFibroblastsBlotting NorthernHematopoietic Stem CellsMolecular biologyImmunohistochemistryReceptors Interleukin-6HaematopoiesisGene Expression RegulationLiverSolubilityHematopoiesis Extramedullarybiology.proteinSpleenExperimental hematology
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Involvement of protein kinase Cdelta in contact-dependent inhibition of growth in human and murine fibroblasts.

2001

There is evidence that protein kinase C delta (PKCdelta) is a tumor suppressor, although its physiological role has not been elucidated so far. Since important anti-proliferative signals are mediated by cell-cell contacts we studied whether PKCdelta is involved in contact-dependent inhibition of growth in human (FH109) and murine (NIH3T3) fibroblasts. Cell-cell contacts were imitated by the addition of glutardialdehyde-fixed cells to sparsely seeded fibroblasts. Downregulation of the PKC isoforms alpha, delta, epsilon, and mu after prolonged treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.1 microM) resulted in a significant release from contact-inhibition in FH109 cells. Bryosta…

Cancer ResearchTime FactorsBryostatin 1ImmunoprecipitationActive Transport Cell NucleusDown-RegulationBiologychemistry.chemical_compoundFixativesLactonesMiceDownregulation and upregulationGeneticsmedicineAnimalsHumansProtein IsoformsBenzopyransEnzyme InhibitorsFibroblastProtein kinase AMolecular BiologyProtein kinase CProtein Kinase CChemotaxisCell CycleAcetophenones3T3 CellsFibroblastsBryostatinsMolecular biologyBlotIsoenzymesProtein Kinase C-deltamedicine.anatomical_structurechemistryGlutaralTetradecanoylphorbol AcetateMacrolidesMitogensRottlerinCell DivisionProtein BindingOncogene
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Partial restoration of pre-transformation levels of lysyl oxidase and transin mRNAs in phenotypic ras revertants.

1995

Neoplastic transformation mediated by ras oncogenes is associated with deregulated expression of genes encoding, for example, various proteases, lysyl oxidase, and smooth-muscle α-actin. To define the role of these genes in the initiation or maintenance of the ras-transformed state, we compared their steady-state mRNA levels in two different sets of preneoplastic fibroblast lines, ras-transformed clones, and phenotypic revertants derived from them. Compared with the preneoplastic fibroblasts, the ras-transformed derivatives exhibited elevated levels of cathepsin L (major excreted protein), transin (stromelysin I, matrix metalloproteinase–3), and collagenase I (matrix metalloproteinase–1) mR…

Cancer ResearchTranscription GeneticCathepsin LBlotting WesternGene ExpressionLysyl oxidaseCell LineCathepsin LProtein-Lysine 6-OxidaseProto-Oncogene Proteins c-mycDownregulation and upregulationEndopeptidasesmedicineAnimalsNeoplastic transformationCollagenasesRNA MessengerFibroblastMolecular BiologyGeneMessenger RNAbiologyMetalloendopeptidasesPhenotypeMolecular biologyCathepsinsNeoplasm ProteinsRatsCysteine Endopeptidasesmedicine.anatomical_structureCell Transformation NeoplasticGenes rasPhenotypebiology.proteinMatrix Metalloproteinase 3Matrix Metalloproteinase 1Precancerous ConditionsMolecular carcinogenesis
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Parthenolide generates reactive oxygen species and autophagy in MDA-MB231 cells. A soluble parthenolide analogue inhibits tumour growth and metastasi…

2013

Triple-negative breast cancers (TNBCs) are clinically aggressive forms associated with a poor prognosis. We evaluated the cytotoxic effect exerted on triple-negative MDA-MB231 breast cancer cells both by parthenolide and its soluble analogue dimethylamino parthenolide (DMAPT) and explored the underlying molecular mechanism. The drugs induced a dose- and time-dependent decrement in cell viability, which was not prevented by the caspase inhibitor z-VAD-fmk. In particular in the first hours of treatment (1–3 h), parthenolide and DMAPT strongly stimulated reactive oxygen species (ROS) generation. The drugs induced production of superoxide anion by activating NADPH oxidase. ROS generation caused…

Cancer ResearchautophagyCell SurvivalparthenolideFas-Associated Death Domain ProteinImmunologyCASP8 and FADD-Like Apoptosis Regulating ProteinBreast Neoplasmsparthenolide; ROS; NOX; autophagy; breast cancer xenograft.MiceCellular and Molecular Neurosciencechemistry.chemical_compoundDownregulation and upregulationCell Line TumorSettore BIO/10 - BiochimicaAnimalsHumansParthenolidePropidium iodidebreast cancer xenograftMembrane Potential Mitochondrialchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologybreast cancer xenograft.SuperoxideNF-kappa BRNA-Binding ProteinsROSCell BiologyNOXXenograft Model Antitumor AssaysMolecular biologyNuclear Pore Complex ProteinsVascular endothelial growth factorchemistryCell cultureCancer researchbiology.proteinCalciumFemaleOriginal ArticleReactive Oxygen SpeciesSesquiterpenes
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Abstract 968: β-catenin plays an important role in lung tumor development induced by EGFR mutations

2014

Abstract The discovery of somatic mutations in epidermal growth factor receptor (EGFR) and the development of EGFR tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib, have revolutionized treatment for non-small cell lung cancer (NSCLC). Resistance to TKIs emerges in almost all patients, but currently no effective treatment is available.Therefore, novel strategies to either prevent or overcome resistance are sorely needed. Here we show that β-catenin is essential for development of EGFR mutated lung cancers. We found that β-catenin was upregulated, translocated to the nucleus, and subsequently activated in both EGFR mutated lung cancer cell lines and EGFR mutation driven lung…

Cancer Researchbiologybusiness.industryCancermedicine.diseasemedicine.disease_causerespiratory tract diseasesGefitinibOncologyDownregulation and upregulationCateninImmunologyCancer researchbiology.proteinMedicineEpidermal growth factor receptorErlotinibbusinessLung cancerCarcinogenesismedicine.drugCancer Research
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Medication for Acromegaly Reduces Expression of MUC16, MACC1 and GRHL2 in Pituitary Neuroendocrine Tumour Tissue

2021

Acromegaly is a disease mainly caused by pituitary neuroendocrine tumor (PitNET) overproducing growth hormone. First-line medication for this condition is the use of somatostatin analogs (SSAs), that decrease tumor mass and induce antiproliferative effects on PitNET cells. Dopamine agonists (DAs) can also be used if SSA treatment is not effective. This study aimed to determine differences in transcriptome signatures induced by SSA/DA therapy in PitNET tissue. We selected tumor tissue from twelve patients with somatotropinomas, with half of the patients receiving SSA/DA treatment before surgery and the other half treatment naive. Transcriptome sequencing was then carried out to identify diff…

Cancer Researchbusiness.industrysomatostatin/dopamine (SSA/DA) therapynext generation sequencing (NGS)medicine.disease_causemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282TranscriptomeExtracellular matrixSomatostatinOncologyDownregulation and upregulationDopamineGene expressionAcromegalyCancer researchMedicineacromegalysomatotropinomabusinessCarcinogenesistranscriptomeOriginal Researchmedicine.drugFrontiers in Oncology
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Ethanol-Mediated Stress Promotes Autophagic Survival and Aggressiveness of Colon Cancer Cells via Activation of Nrf2/HO-1 Pathway

2019

Epidemiological studies suggest that chronic alcohol consumption is a lifestyle risk factor strongly associated with colorectal cancer development and progression. The aim of the present study was to examine the effect of ethanol (EtOH) on survival and progression of three different colon cancer cell lines (HCT116, HT29, and Caco-2). Our data showed that EtOH induces oxidative and endoplasmic reticulum (ER) stress, as demonstrated by reactive oxygen species (ROS) and ER stress markers Grp78, ATF6, PERK and, CHOP increase. Moreover, EtOH triggers an autophagic response which is accompanied by the upregulation of beclin, LC3-II, ATG7, and p62 proteins. The addition of the antioxidant N-acetyl…

Cancer Researchendocrine systemautophagyHO-1Colon cancer cellmedicine.disease_causelcsh:RC254-282ArticleNrf2Downregulation and upregulationSettore BIO/10 - Biochimicamedicinechemistry.chemical_classificationReactive oxygen speciesATF6Endoplasmic reticulumAutophagylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHeme oxygenaseOncologychemistryCancer researchUnfolded protein responseER strecolon cancer cellsethanolMMPsER stressOxidative stressCancers
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