Search results for "MAI"

showing 10 items of 6279 documents

The role of hydrophobic matching on transmembrane helix packing in cells

2017

Folding and packing of membrane proteins are highly influenced by the lipidic component of the membrane. Here, we explore how the hydrophobic mismatch (the difference between the hydrophobic span of a transmembrane protein region and the hydrophobic thickness of the lipid membrane around the protein) influences transmembrane helix packing in a cellular environment. Using a ToxRED assay in Escherichia coli and a Bimolecular Fluorescent Complementation approach in human-derived cells complemented by atomistic molecular dynamics simulations we analyzed the dimerization of Glycophorin A derived transmembrane segments. We concluded that, biological membranes can accommodate transmembrane homo-di…

Cancer ResearchPhysiologyCèl·luleslcsh:Medicine010402 general chemistry114 Physical sciences01 natural sciencesBiochemistry Genetics and Molecular Biology (miscellaneous)03 medical and health sciencesHydrophobic mismatchhydrophobic matchhelix packingLipid bilayerlcsh:QH301-705.5030304 developmental biology0303 health sciencesChemistrylcsh:RGlycophorin AProteïnes de membranaGlycophorin ABiological membranetransmembrane domain dimerizationmembrane protein foldingTransmembrane protein0104 chemical sciencesFolding (chemistry)Transmembrane domainMembranelcsh:Biology (General)Membrane proteinBiophysicsMolecular MedicinemismatchResearch ArticleCell Stress
researchProduct

Chemotherapy-induced apoptosis in hepatocellular carcinoma involves the p53 family and is mediatedviathe extrinsic and the intrinsic pathway

2010

We investigated the downstream mechanisms by which chemotherapeutic drugs elicit apoptosis in hepatocellular carcinoma (HCC). Genomic signatures of HCC cell lines treated with different chemotherapeutic drugs were obtained. Analyses of apoptosis pathways were performed and RNA interference was used to evaluate the role of the p53 family. Endogenous p53, p63 and p73 were upregulated in response to DNA damage by chemotherapeutic drugs. Blocking p53 family function led to chemoresistance in HCC. Stimulation and blocking experiments of the CD95-, the TNF- and the TRAIL-receptor systems revealed that cytotoxic drugs, via the p53 family members as transactivators, can trigger expression of each o…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTumor suppressor geneDNA damagetumor suppressor protein p53membrane proteinsoligonucleotide array sequence analysiscarcinomaBiologyhepatocellularfas-associated death domain proteinAPAF1humansMembrane Potential Mitochondrialhep G2 cellsbleomycinliver neoplasmsSettore BIO/11apoptosisPrognosismitochondrialFas receptorcaspasesOncologyApoptosisbiology.proteinCancer researchMdm2membrane potentialSignal transductionPrognosis; bleomycin; caspases; membrane potential mitochondrial; oligonucleotide array sequence analysis; tumor suppressor protein p53; membrane proteins; fas-associated death domain protein; humans; liver neoplasms; hep G2 cells; apoptosis; carcinoma hepatocellularInternational Journal of Cancer
researchProduct

Resistance to diverse apoptotic triggers in multidrug resistant HL60 cells and its possible relationship to the expression of P-glycoprotein, Fas and…

2002

We studied the human HL60 leukemia cell line and its multidrug resistant (MDR) variant HL60R. In contrast to the HL60, HL60R showed an inability to undergo apoptosis from doxorubicin (Dox) or other different stimuli, including cisplatin, Fas ligation and serum withdrawal. HL60R cells lost surface Fas expression, but we found no evidence that Fas/FasL mediates the apoptotic effects of Dox in HL60. P-glycoprotein (P-gp) did not seem to play a major role as a specific inhibitor of apoptosis. In fact, the P-gp inhibitor verapamil reversed only partially the resistance to Dox-induced apoptosis of the MDR cells. In addition, it did not modify the rate of apoptosis induced from the other stimuli i…

Cancer ResearchProgrammed cell deathTime FactorsChromosomal Proteins Non-HistoneSurvivinDown-RegulationAntineoplastic AgentsApoptosisHL-60 CellsNerve Tissue ProteinsBiologyInhibitor of apoptosisFas ligandInhibitor of Apoptosis ProteinsInhibitory Concentration 50SurvivinTumor Cells CulturedHumansATP Binding Cassette Transporter Subfamily B Member 1RNA Messengerfas ReceptorP-glycoproteinInhibitor of apoptosis domainCaspase 3Reverse Transcriptase Polymerase Chain ReactionProteinsFlow CytometryNeuronal Apoptosis-Inhibitory ProteinNeoplasm ProteinsCell biologyProto-Oncogene Proteins c-bcl-2OncologyDoxorubicinDrug Resistance NeoplasmApoptosisCaspasesbiology.proteinInsect ProteinsNAIPCisplatinMicrotubule-Associated ProteinsCancer Letters
researchProduct

MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts

2013

The oncogenes MYCN and survivin (BIRC5) maintain aggressiveness of diverse cancers including sarcomas. To investigate whether these oncogenes cooperate in initial malignant transformation, we transduced them into Rat-1 fibroblasts. Indeed, survivin enhanced MYCN-driven contact-uninhibited and anchorage-independent growth in vitro. Importantly, upon subcutaneous transplantation into mice, cells overexpressing both instead of either one of the oncogenes generated tumors with shortened latency, marked anaplasia and an increased proliferation-to-apoptosis ratio resulting in accelerated growth. Mechanistically, the increased tumorigenicity was associated with an enhanced Warburg effect and a hyp…

Cancer ResearchSurvivinBlotting WesternApoptosisBiologyReal-Time Polymerase Chain ReactionN-Myc Proto-Oncogene ProteinInhibitor of Apoptosis ProteinsMalignant transformationImmunoenzyme TechniquesMiceAdenosine TriphosphateSurvivinmedicineAnimalsHumansLactic AcidRNA MessengerneoplasmsAnaplasiaCells CulturedCell ProliferationHomeodomain ProteinsOncogene ProteinsN-Myc Proto-Oncogene ProteinReverse Transcriptase Polymerase Chain ReactionCell growthNuclear ProteinsGeneral MedicineFibroblastsWarburg effectCell HypoxiaRatsTransplantationCell Transformation NeoplasticGlucoseHypoxia-inducible factorsCancer researchmedicine.symptomGlycolysisCarcinogenesis
researchProduct

Pharmacologic activation of p53 elicits Bax-dependent apoptosis in the absence of transcription

2003

AbstractRecent efforts to develop pharmacologic agents that restore function to mutant forms of p53 hold significant promise in cancer therapy. Here, we examine the effects of such pharmacologic activation of p53 function using a small molecule, PRIMA-1, and a model system employing a p53 protein fused to a mutant steroid binding domain of the murine estrogen receptor (p53ERtam) that renders it responsive only in the presence of 4-hydroxytamoxifen. In either case, p53 activation triggered apoptosis that was not inhibited by the presence of macromolecular synthesis inhibitors. This p53-induced, transcription-independent apoptosis is Bax dependent, proceeds in the absence of a nucleus, and in…

Cancer ResearchTranscription GeneticRecombinant Fusion ProteinsMutantEstrogen receptorApoptosis03 medical and health sciencesMice0302 clinical medicineBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedAnimalsHumansCloning MolecularReceptorCells Cultured030304 developmental biologybcl-2-Associated X ProteinCell NucleusProtein Synthesis Inhibitors0303 health sciencesAza CompoundsbiologyCytochrome cCytochromes cCell BiologyFibroblastsBridged Bicyclo Compounds Heterocyclic3. Good healthCell biologyTransport proteinMitochondriaProtein TransportTamoxifenProto-Oncogene Proteins c-bcl-2Receptors EstrogenOncologyApoptosis030220 oncology & carcinogenesisMutationbiology.proteinTumor Suppressor Protein p53Binding domainCancer Cell
researchProduct

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
researchProduct

Comprehensive Analysis of VEGFR2 Expression in HPV-Positive and -Negative OPSCC Reveals Differing VEGFR2 Expression Patterns

2021

VEGF signaling regulated by the vascular endothelial growth factor receptor 2 (VEGFR2) plays a decisive role in tumor angiogenesis, initiation and progression in several tumors including HNSCC. However, the impact of HPV-status on the expression of VEGFR2 in OPSCC has not yet been investigated, although HPV oncoproteins E6 and E7 induce VEGF-expression. In a series of 56 OPSCC with known HPV-status, VEGFR2 expression patterns were analyzed both in blood vessels from tumor-free and tumor-containing regions and within tumor cells by immunohistochemistry using densitometry. Differences in subcellular colocalization of VEGFR2 with endothelial, tumor and stem cell markers were determined by doub…

Cancer Researchcancer stem cellAngiogenesisNeoplasms. Tumors. Oncology. Including cancer and carcinogensKinase insert domain receptorBiologyrespiratory systemStem cell markerArticlemedicine.anatomical_structureOncologyCancer stem cellvascular endothelial growth factor receptor 2Cancer cellCancer researchmedicinecardiovascular systemoropharyngeal squamous cell carcinomaImmunohistochemistryAutocrine signallinghuman papillomavirusRC254-282Blood vesselcirculatory and respiratory physiology
researchProduct

Mammary-derived growth inhibitor (MDGI) interacts with integrin α-subunits and suppresses integrin activity and invasion

2010

The majority of mortality associated with cancer is due to formation of metastases from the primary tumor. Adhesion mediated by different integrin heterodimers has an important role during cell migration and invasion. Protein interactions with the β1-integrin cytoplasmic tail are known to influence integrin affinity for extracellular ligands, but regulating binding partners for the α-subunit cytoplasmic tails have remained elusive. In this study, we show that mammary-derived growth inhibitor (MDGI) (also known as FABP-3 or H-FABP) binds directly to the cytoplasmic tail of integrin α-subunits and its expression inhibits integrin activity. In breast cancer cell lines, MDGI expression correlat…

Cancer Researchmedicine.disease_causemigrationCD49cCollagen receptor0302 clinical medicineCell Movement0303 health sciencesCell migrationMiddle Agedinvasion3. Good healthCell biologyExtracellular MatrixadhesionIntegrin alpha MMDGI030220 oncology & carcinogenesis/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingIntegrin beta 6FemaleFatty Acid Binding Protein 3Integrin alpha Chainsmedicine.medical_specialtyintegrinIntegrinMolecular Sequence DataBreast NeoplasmsBiologyFatty Acid-Binding ProteinsCollagen Type IDisease-Free Survival03 medical and health sciencesbreast cancerSDG 3 - Good Health and Well-beingInternal medicineCell Line TumorGeneticsmedicineHumansNeoplasm InvasivenessProtein Interaction Domains and MotifsAmino Acid SequenceMolecular Biology030304 developmental biologyFibronectinsFibronectinEndocrinologybiology.proteinCarcinogenesisOncogene
researchProduct

Intratumoral Heterogeneity in EGFR-Mutant NSCLC Results in Divergent Resistance Mechanisms in Response to EGFR Tyrosine Kinase Inhibition

2015

Abstract Non–small cell lung cancers (NSCLC) that have developed resistance to EGF receptor (EGFR) tyrosine kinase inhibitor (TKI), including gefitinib and erlotinib, are clinically linked to an epithelial-to-mesenchymal transition (EMT) phenotype. Here, we examined whether modulating EMT maintains the responsiveness of EGFR-mutated NSCLCs to EGFR TKI therapy. Using human NSCLC cell lines harboring mutated EGFR and a transgenic mouse model of lung cancer driven by mutant EGFR (EGFR-Del19-T790M), we demonstrate that EGFR inhibition induces TGFβ secretion followed by SMAD pathway activation, an event that promotes EMT. Chronic exposure of EGFR-mutated NSCLC cells to TGFβ was sufficient to ind…

Cancer Researchmedicine.drug_classCellBiologymedicine.diseaseArticleTyrosine-kinase inhibitorrespiratory tract diseasesmedicine.anatomical_structureGefitinibOncologyProtein kinase domainImmunologymedicineCancer researchEpithelial–mesenchymal transitionErlotinibSignal transductionLung cancerneoplasmsmedicine.drugCancer Research
researchProduct

Post-Induction Management in Patients With Left-Sided RAS and BRAF Wild-Type Metastatic Colorectal Cancer Treated With First-Line Anti-EGFR-Based Dou…

2021

BackgroundFew data regarding post-induction management following first-line anti-epidermal growth factor receptor (EGFR)-based doublet regimens in patients with left-sided RAS/BRAF wild-type metastatic colorectal cancer (mCRC) are available.MethodsThis multicenter, retrospective study aimed at evaluating clinicians’ attitude, and the safety and effectiveness of post-induction strategies in consecutive patients affected by left-sided RAS/BRAF wild-type mCRC treated with doublet chemotherapy plus anti-EGFR as first-line regimen, who did not experience disease progression within 6 months from induction initiation, at 21 Italian and 1 Spanish Institutions. The measured clinical outcomes were: p…

Cancer Researchmedicine.medical_specialtyColorectal cancerPopulationGastroenterologymaintenanceFOLFIRIFOLFOXInternal medicinecetuximabmedicineAdverse effecteducationRC254-282education.field_of_studybusiness.industryMCRCNeoplasms. Tumors. Oncology. Including cancer and carcinogensRetrospective cohort studymedicine.diseaseRegimenFOLFOXOncologyCohortFOLFIRIbusinesspanitumumabmedicine.drugFrontiers in Oncology
researchProduct