Search results for "PAR-4"

showing 3 items of 3 documents

Involvement of PAR-4 in Cannabinoid-Dependent Sensitization of Osteosarcoma Cells to TRAIL-Induced Apoptosis

2014

The synthetic cannabinoid WIN 55,212-2 is a potent cannabinoid receptor agonist with anticancer potential. Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells. Results show that WIN induced G2/M cell cycle arrest, which was associated with the induction of the main markers of ER stress (GRP78, CHOP and TRB3). In treated cells we also observed the conversion of the cytosolic form of the autophagosome marker LC3-I into LC3-II (the lipidated form located on the autophagosome membrane) and the enhanced incorporation of monodansylcadaverine and acridine orange, two markers of t…

AutophagosomeautophagyProgrammed cell deathCannabinoids ER stress autophagy TRAIL osteosarcoma cells GRP78/PAR-4 complex.Cannabinoid receptorMorpholinesCellApoptosisTRAILNaphthalenesBiologyGRP78/PAR-4 complex.Applied Microbiology and BiotechnologyTNF-Related Apoptosis-Inducing LigandCadaverineCell Line TumorSettore BIO/10 - BiochimicamedicineHumansRNA Small InterferingEndoplasmic Reticulum Chaperone BiPMolecular BiologyHeat-Shock ProteinsEcology Evolution Behavior and SystematicsCell ProliferationCannabinoid Receptor AgonistsOsteosarcomaCannabinoidsAutophagyCell Cycle Checkpointsosteosarcoma cellsCell BiologyCell cycleEndoplasmic Reticulum StressAcridine OrangeBenzoxazinesCell biologymedicine.anatomical_structureApoptosisAutophagosome membraneApoptosis Regulatory ProteinsER stressMicrotubule-Associated ProteinsResearch PaperDevelopmental Biology
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Regulation of the proapoptotic functions of prostate apoptosis response-4 (Par-4) by casein kinase 2 in prostate cancer cells

2013

International audience; The proapoptotic protein, prostate apoptosis response-4 (Par-4), acts as a tumor suppressor in prostate cancer cells. The serine/threonine kinase casein kinase 2 (CK2) has a well-reported role in prostate cancer resistance to apoptotic agents or anticancer drugs. However, the mechanistic understanding on how CK2 supports survival is far from complete. In this work, we demonstrate both in rat and humans that (i) Par-4 is a new substrate of the survival kinase CK2 and (ii) phosphorylation by CK2 impairs Par-4 proapoptotic functions. We also unravel different levels of CK2-dependent regulation of Par-4 between species. In rats, the phosphorylation by CK2 at the major si…

MaleCancer Researchanimal structuresCK2[SDV]Life Sciences [q-bio]ImmunologyAmino Acid MotifsPAWR[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Biology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biology[SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and NephrologyCellular and Molecular NeuroscienceProstate cancer[SDV.CAN] Life Sciences [q-bio]/CancerProstateCell Line Tumor[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]medicineAnimalsHumansCasein Kinase IIComputingMilieux_MISCELLANEOUSGene knockdownKinasephosphorylationfungita1182apoptosisProstatic Neoplasms[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCell Biologymedicine.diseaseprostate cancer[SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and NephrologyRatsmedicine.anatomical_structureApoptosisembryonic structuresCancer researchPhosphorylationOriginal ArticleCasein kinase 2Apoptosis Regulatory ProteinsPar-4
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Ruolo citotossico del cannabinoide sintetico WIN55,212-2 in cellule di osteosarcoma MG63: coinvolgimento della proteina SPARC.

Il cannabinoide sintetico WIN 55,212-2 è un potente agonista sintetico del recettore per i cannabinoidi con spiccate potenzialità antitumorali. Gli esperimenti riportati in questa tesi sono stati condotti per delineare gli effetti indotti dal WIN sulla proliferazione, la migrazione e la sensibilizzazione alla morte indotta dalla citochina TRAIL in cellule di osteosarcoma umano MG63. I risultati ottenuti mostrano che il WIN induce un blocco del ciclo cellulare in fase G2/M che è associato all’induzione dei principali markers di ER stress (GRP78, CHOP e TRB3). Nelle cellule trattate abbiamo inoltre osservato la conversione della forma citosolica del marker autofagosomale LC3-I in LC3-II (la f…

meccanismi di morte cellularemiR-29-b1Settore BIO/10 - BiochimicaMG63ER streSPARCcannabinoidiPAR-4
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