We are analyzing https://link.springer.com/article/10.1007/s10495-006-8896-3.

Title:
Troglitazone sensitizes tumor cells to TRAIL-induced apoptosis via down-regulation of FLIP and Survivin | Apoptosis
Description:
Induction of apoptosis by the death ligand TRAIL might be a promising therapeutic approach in cancer therapy. However, since not all tumor cells are sensitive to TRAIL, there is a need for the development of strategies to overcome TRAIL-resistance. The results of the present study show that the anti-diabetic drug troglitazone sensitizes human glioma and neuroblastoma cells to TRAIL-induced apoptosis. This process is accompanied by a substantial increase of active caspase 8 and active caspase 3, but it is independent of troglitazone
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Keywords {🔍}

article, pubmed, google, scholar, cas, apoptosis, cells, cancer, tumor, flip, trailinduced, troglitazone, protein, survivin, ligand, expression, sensitizes, trail, glioma, cell, access, privacy, cookies, content, roth, human, malignant, information, publish, research, search, neuroblastoma, receptor, levels, resistance, nat, res, peroxisome, proliferatoractivated, data, log, journal, schultze, böck, eckert, wilfried, death, therapy, caspase, open,

Topics {✒️}

peroxisome proliferator-activated receptor-gamma gcn2/trail-r2/caspase-8 apoptotic pathway anti-apoptotic flice-inhibitory protein bcl-xl/bcl-2 functions independently otmar wiestler & wilfried roth month download article/chapter nuclear receptor ppar-γ anticancer drug-induced apoptosis casitas b-lineage lymphoma article apoptosis aims smac agonists sensitize related subjects overcome trail-resistance full article pdf trail-induced apoptosis apoptosis protein survivin temozolomide sensitizes stem glioma cell survival privacy choices/manage cookies tumor cells promising therapeutic approach multiple tumour types breast cancer cells prostate cancer cells death ligand trail thiazolidenediones mediate apoptosis trail receptor cell cycle arrest reed-sternberg cells promising experimental therapy reducing survivin levels neuroblastoma cells correlates german cancer aid apo2l/trail protein expression levels wilfried roth article schultze check access instant access induces cell death european economic area present study show reactive oxygen species human transcriptomes cyclin d3 repression max eder program mrna expression levels conditions privacy policy synthetic triterpenoids cooperate article log

Questions {❓}

Rieger J, Naumann U, Glaser T, Ashkenazi A, Weller M (1998) APO2 ligand: a novel lethal weapon against malignant glioma?

Schema {🗺️}

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         description:Induction of apoptosis by the death ligand TRAIL might be a promising therapeutic approach in cancer therapy. However, since not all tumor cells are sensitive to TRAIL, there is a need for the development of strategies to overcome TRAIL-resistance. The results of the present study show that the anti-diabetic drug troglitazone sensitizes human glioma and neuroblastoma cells to TRAIL-induced apoptosis. This process is accompanied by a substantial increase of active caspase 8 and active caspase 3, but it is independent of troglitazone's effects on the nuclear receptor PPAR-γ. Troglitazone induces a pronounced reduction in protein expression levels of the anti-apoptotic FLICE-inhibitory protein (FLIP) without affecting FLIP mRNA levels. Further, protein and mRNA expression levels of the anti-apoptotic protein Survivin significantly decrease upon treatment with troglitazone. Moreover, sensitization to TRAIL is partly accompanied by an up-regulation of the TRAIL receptor, TRAIL-R2. A combined treatment with troglitazone and TRAIL might be a promising experimental therapy because troglitazone sensitizes tumor cells to TRAIL-induced apoptosis via various mechanisms, thereby minimizing the risk of acquired tumor cell resistance.
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         dateModified:2006-06-27T00:00:00Z
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      headline:Troglitazone sensitizes tumor cells to TRAIL-induced apoptosis via down-regulation of FLIP and Survivin
      description:Induction of apoptosis by the death ligand TRAIL might be a promising therapeutic approach in cancer therapy. However, since not all tumor cells are sensitive to TRAIL, there is a need for the development of strategies to overcome TRAIL-resistance. The results of the present study show that the anti-diabetic drug troglitazone sensitizes human glioma and neuroblastoma cells to TRAIL-induced apoptosis. This process is accompanied by a substantial increase of active caspase 8 and active caspase 3, but it is independent of troglitazone's effects on the nuclear receptor PPAR-γ. Troglitazone induces a pronounced reduction in protein expression levels of the anti-apoptotic FLICE-inhibitory protein (FLIP) without affecting FLIP mRNA levels. Further, protein and mRNA expression levels of the anti-apoptotic protein Survivin significantly decrease upon treatment with troglitazone. Moreover, sensitization to TRAIL is partly accompanied by an up-regulation of the TRAIL receptor, TRAIL-R2. A combined treatment with troglitazone and TRAIL might be a promising experimental therapy because troglitazone sensitizes tumor cells to TRAIL-induced apoptosis via various mechanisms, thereby minimizing the risk of acquired tumor cell resistance.
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         Apoptosis
         Brain tumors
         Troglitazone
         FLIP
         Survivin
         Cancer Research
         Cell Biology
         Oncology
         Biochemistry
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         Virology
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