0000000000729553

AUTHOR

Michela Garofalo

showing 2 related works from this author

PED is overexpressed and mediates TRAIL resistance in human non-small cell lung cancer

2008

PED (phosphoprotein enriched in diabetes) is a death-effector domain (DED) family member with a broad anti-apoptotic action. PED inhibits the assembly of the death-inducing signalling complex (DISC) of death receptors following stimulation. Recently, we reported that the expression of PED is increased in breast cancer cells and determines the refractoriness of these cells to anticancer therapy. In the present study, we focused on the role of PED in non-small cell lung cancer (NSCLC), a tumour frequently characterized by evasion of apoptosis and drug resistance. Immunohistochemical analysis of a tissue microarray, containing 160 lung cancer samples, indicated that PED was strongly expressed …

MaleProgrammed cell deathLung NeoplasmsNecrosisProtein Array AnalysisBiologyTransfectionTNF-Related Apoptosis-Inducing LigandCarcinoma Non-Small-Cell LungCell Line TumormedicineHumansGene silencingRNA Small InterferingLung cancerAgedAged 80 and overTissue microarrayAKTapoptosisIntracellular Signaling Peptides and ProteinsArticlesCell BiologyTransfectionMiddle AgedPhosphoproteinsmedicine.diseaseMolecular biologyRecombinant ProteinsUp-Regulationlung cancerReceptors TNF-Related Apoptosis-Inducing LigandDrug Resistance NeoplasmCell cultureApoptosisMolecular MedicineFemalemedicine.symptomApoptosis Regulatory ProteinsJournal of Cellular and Molecular Medicine
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PED Mediates AKT-Dependent Chemoresistance in Human Breast Cancer Cells

2005

Abstract Killing of tumor cells by cytotoxic therapies, such as chemotherapy or gamma-irradiation, is predominantly mediated by the activation of apoptotic pathways. Refractoriness to anticancer therapy is often due to a failure in the apoptotic pathway. The mechanisms that control the balance between survival and cell death in cancer cells are still largely unknown. Tumor cells have been shown to evade death signals through an increase in the expression of antiapoptotic molecules or loss of proapoptotic factors. We aimed to study the involvement of PED, a molecule with a broad antiapoptotic action, in human breast cancer cell resistance to chemotherapeutic drugs–induced cell death. We show…

EXPRESSIONAdultCancer ResearchProgrammed cell deathmedicine.medical_treatmentINHIBITIONApoptosisBreast NeoplasmsProtein Serine-Threonine KinasesDNA AntisenseACTIVATIONBreast cancerTransduction GeneticCell Line TumorProto-Oncogene ProteinsComplementary DNAmedicineHumansCytotoxic T cellPROTEIN-KINASE-CProtein kinase BAgedNeoplasm StagingChemotherapybusiness.industryDEATHIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesIN-VITROCHEMOTHERAPYMiddle AgedPhosphoproteinsmedicine.diseasePED/PEA-15Up-RegulationEnzyme ActivationOncologyDrug Resistance NeoplasmApoptosisCancer cellImmunologyCancer researchFemalePTEN GENEApoptosis Regulatory ProteinsbusinessProto-Oncogene Proteins c-aktCancer Research
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