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• W1991178756 abstract "Mechanisms underlying interactions between the proteasome inhibitor bortezomib and small molecule Bcl-2 antagonists were examined in GC- and ABC-type human DLBCL (diffuse lymphocytic B-cell lymphoma) cells. Concomitant or sequential exposure to non- or minimally toxic concentrations of bortezomib or other proteasome inhibitors and either HA14-1 or gossypol resulted in a striking increase in Bax/Bak conformational change/translocation, cytochrome c release, caspase activation, and synergistic induction of apoptosis in both GC- and ABC-type cells. These events were associated with a sharp increase in activation of the stress kinase JNK and evidence of ER stress induction (e.g., eIF2α phosphorylation, activation of caspases-2 and - 4, and Grp78 upregulation). Pharmacologic or genetic (e.g., shRNA knockdown ) interruption of JNK signaling attenuated HA14-1/bortezomib lethality and ER stress induction. Genetic disruption of the ER stress pathway (e.g., in cells expressing caspase -4 shRNA or DN-eIF2α) significantly attenuated lethality. The toxicity of this regimen was independent of ROS generation. Finally, HA14-1 significantly increased bortezomib-mediated JNK activation, ER stress induction, and lethality in bortezomib-resistant cells. Collectively these findings indicate that small molecule Bcl-2 antagonists promote bortezomib-mediated mitochondrial injury and lethality in DLBCL cells in association with enhanced JNK activation and ER stress induction. They also raise the possibility that such a strategy may be effective in different DLBCL sub- types (e.g., GC- or ABC), and in bortezomib-resistant disease." @default.
• W1991178756 created "2016-06-24" @default.
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• W1991178756 date "2009-05-01" @default.
• W1991178756 modified "2023-09-27" @default.
• W1991178756 title "BCL-2 antagonists interact synergistically with bortezomib in DLBCL cells in association with JNK activation and induction of ER stress" @default.
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• W1991178756 doi "https://doi.org/10.4161/cbt.8.9.8131" @default.
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