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Keywords {🔍}

article, cells, erk, proliferation, glioma, activation, trailinduced, apoptosis, cell, privacy, cookies, content, trail, human, access, analysis, information, publish, research, search, bumbasirevic, data, log, journal, life, induces, february, vilimanovich, resistant, cflip, discover, author, springer, optional, personal, parties, policy, find, track, cellular, molecular, sciences, cfliplmediated, published, cite, explore, time, growth, trailresistant, western,

Topics {✒️}

tnf-related apoptosis-inducing ligand trail-induced erk1/2 activation c-flipl-mediated activation trail-induced cell growth caspase-8 inhibitor c-flipl trail-resistant glioma cells trail-induced apoptosis casitas b-lineage lymphoma month download article/chapter trail induces proliferation retinoblastoma protein phosphorylation resistant glioma cells human glioma cells related subjects resistant cells occurred privacy choices/manage cookies full article pdf induces apoptosis european economic area scope submit manuscript western blot analysis temozolomide sensitizes stem early event required conditions privacy policy accepting optional cookies cell proliferation check access instant access article cellular journal finder publish c-cbl article log erk1/2 proteins erk1/2 kinases life sci article number 814 glioma spheres 1007/s00018-008-7513-8 keywords human glioblastoma article cite privacy policy personal data author correspondence article vilimanovich books a trail optional cookies usage analysis manage preferences subscription content

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         headline:TRAIL induces proliferation of human glioma cells by c-FLIPL-mediated activation of ERK1/2
         description:TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in TRAIL-sensitive human malignant glioma cells. We show for the first time that TRAIL stimulates cell growth in TRAIL-resistant glioma cells. TRAIL-induced cell growth in resistant cells occurred through increased cell cycle progression as determined by flow cytometry and Western blot analysis of retinoblastoma protein phosphorylation. Western blot analysis of TRAIL-treated resistant cells revealed phosphorylation of ERK1/2 proteins and in vitro kinase analysis confirmed the activation of the ERK1/2 kinases. Inhibition of MEK1 eliminated both TRAIL-induced ERK1/2 activation and cell proliferation. In addition, siRNA inhibition of c-FLIP expression eliminates TRAIL-induced ERK1/2 activation and proliferation. Furthermore, overexpression of c-FLIPL potentiates TRAIL-induced ERK1/2 activation and proliferation of resistant glioma cells. Our results have shown for the first time that TRAIL-induced ERK1/2 activation and proliferation of TRAIL-resistant human glioma cells is dependent upon the expression of the long form of the caspase-8 inhibitor c-FLIPL.
         datePublished:2008-02-01T00:00:00Z
         dateModified:2008-02-01T00:00:00Z
         pageStart:814
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            apoptosis
            proliferation
            c-FLIP
            ERK1/2
            glioma
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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               name:U. Vilimanovich
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                        name:Institute of Histology and Embryology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia
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      headline:TRAIL induces proliferation of human glioma cells by c-FLIPL-mediated activation of ERK1/2
      description:TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in TRAIL-sensitive human malignant glioma cells. We show for the first time that TRAIL stimulates cell growth in TRAIL-resistant glioma cells. TRAIL-induced cell growth in resistant cells occurred through increased cell cycle progression as determined by flow cytometry and Western blot analysis of retinoblastoma protein phosphorylation. Western blot analysis of TRAIL-treated resistant cells revealed phosphorylation of ERK1/2 proteins and in vitro kinase analysis confirmed the activation of the ERK1/2 kinases. Inhibition of MEK1 eliminated both TRAIL-induced ERK1/2 activation and cell proliferation. In addition, siRNA inhibition of c-FLIP expression eliminates TRAIL-induced ERK1/2 activation and proliferation. Furthermore, overexpression of c-FLIPL potentiates TRAIL-induced ERK1/2 activation and proliferation of resistant glioma cells. Our results have shown for the first time that TRAIL-induced ERK1/2 activation and proliferation of TRAIL-resistant human glioma cells is dependent upon the expression of the long form of the caspase-8 inhibitor c-FLIPL.
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                     type:PostalAddress
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