We are analyzing https://link.springer.com/article/10.1007/s11064-007-9475-x.

Title:
Ciglitazone Induces Caspase-Independent Apoptosis through Down-Regulation of XIAP and Survivin in Human Glioma Cells | Neurochemical Research
Description:
Induction of apoptosis may be a promising therapeutic approach in cancer therapy. Peroxisome proliferator-activated receptor-γ (PPARγ) agonists induce apoptosis in various cancer cells. However, the molecular mechanism remains to be defined. The present study was undertaken to determine the precise mechanism of cell death induced by ciglitazone, a synthetic PPARγ agonist, in A172 human glioma cells. Ciglitazone resulted in a concentration- and time-dependent apoptotic cell death. Similar results were obtained with troglitazone, another synthetic PPARγ agonist. Ciglitazone induced reactive oxygen species (ROS) generation and ciglitazone-induced cell death was prevented by the antioxidant N-acetylcysteine, suggesting an important role of ROS generation in the ciglitazone-induced cell death. The cell death induced by ciglitazone was inhibited by the PPARγ antagonist GW9662. Although ciglitazone treatment caused a transient activation of extracellular signal-regulated kinase (ERK) and p38, the ciglitazone-induced cell death was not affected by inhibitors of these kinses. Ciglitazone caused a loss of mitochondrial membrane potential and its effect was prevented by N-acetylcysteine and GW9662. The specific inhibitor of caspases-3 DEVD-CHO and the general caspase inhibitor z-DEVD-FMK did not exert the protective effect against the ciglitazone-induced cell death and caspase-3 activity also was not altered by ciglitazone. The ciglitazone-induced cell death was accompanied by down-regulation of XIAP and Survivin, but not by release of apoptosis-inducing factor. Taken together, these findings suggest that down-regulation of XIAP and Survivin may play an active role in mediating a caspase-independent and -PPARγ-dependent cell death induced by ciglitazone in A172 human glioma cells. These data may provide a novel insight into potential therapeutic strategies for treatment of glioblastoma.
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Keywords {🔍}

article, pubmed, google, scholar, cas, cell, apoptosis, cells, death, human, kim, cancer, biol, peroxisome, survivin, ciglitazone, induces, glioma, proliferatoractivated, role, chem, receptor, expression, xiap, mechanism, deoxydeltaprostaglandin, research, downregulation, choi, pparγ, activation, kinase, erk, access, res, mitochondria, pusan, privacy, cookies, content, kang, park, induction, induced, troglitazone, ciglitazoneinduced, mitochondrial, activity, stress, survival,

Topics {✒️}

peroxisome proliferator-activated receptor-gamma peroxisome proliferator-activated receptor-γ peroxisome-proliferator-activated receptors extracellular signal-regulated kinase month download article/chapter reactive oxygen species ciglitazone-induced cell death 14-prostaglandin j2-induced apoptosis jnk-p38 map kinases yong keun kim nf-kappab-dependent mechanism activates nuclear factor-kappab chang hwa choi related subjects mitochondrial apoptosis-inducing factor independent mechanisms malignant b-lineage cells induces cell death population-based studies mitochondrial death/life regulator c-myc gene expression synthetic pparγ agonist troglitazone induces apoptosis full article pdf article kang caspase-independent nuclear receptor ppargamma cell death induced map kinase cascades map kinase pathways mapk-dependent mechanism human glioma cells privacy choices/manage cookies cisplatin-induced apoptosis trail-induced apoptosis caspase 9-interacting sites intracellular oxidative stress agonists induce apoptosis pparγ ligand cell death execution hydrogen peroxide activation apoptosis-inducing factor human cell lines glioma cell survival caspase-mediated cleavage iaps regulates apoptosis human endothelial cells cancer cell lines oligodendrocyte cell line anti-apoptosis gene

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         description:Induction of apoptosis may be a promising therapeutic approach in cancer therapy. Peroxisome proliferator-activated receptor-γ (PPARγ) agonists induce apoptosis in various cancer cells. However, the molecular mechanism remains to be defined. The present study was undertaken to determine the precise mechanism of cell death induced by ciglitazone, a synthetic PPARγ agonist, in A172 human glioma cells. Ciglitazone resulted in a concentration- and time-dependent apoptotic cell death. Similar results were obtained with troglitazone, another synthetic PPARγ agonist. Ciglitazone induced reactive oxygen species (ROS) generation and ciglitazone-induced cell death was prevented by the antioxidant N-acetylcysteine, suggesting an important role of ROS generation in the ciglitazone-induced cell death. The cell death induced by ciglitazone was inhibited by the PPARγ antagonist GW9662. Although ciglitazone treatment caused a transient activation of extracellular signal-regulated kinase (ERK) and p38, the ciglitazone-induced cell death was not affected by inhibitors of these kinses. Ciglitazone caused a loss of mitochondrial membrane potential and its effect was prevented by N-acetylcysteine and GW9662. The specific inhibitor of caspases-3 DEVD-CHO and the general caspase inhibitor z-DEVD-FMK did not exert the protective effect against the ciglitazone-induced cell death and caspase-3 activity also was not altered by ciglitazone. The ciglitazone-induced cell death was accompanied by down-regulation of XIAP and Survivin, but not by release of apoptosis-inducing factor. Taken together, these findings suggest that down-regulation of XIAP and Survivin may play an active role in mediating a caspase-independent and -PPARγ-dependent cell death induced by ciglitazone in A172 human glioma cells. These data may provide a novel insight into potential therapeutic strategies for treatment of glioblastoma.
         datePublished:2007-10-17T00:00:00Z
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