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Desipramine induces apoptosis in rat glioma cells via endoplasmic reticulum stress-dependent CHOP pathway.

Authors: Ma, J  Qiu, Y  Yang, L  Peng, L  Xia, Z  Hou, LN  Fang, C  Qi, H  Chen, HZ 
Citation: Ma J, etal., J Neurooncol. 2011 Jan;101(1):41-8. doi: 10.1007/s11060-010-0237-2. Epub 2010 Jun 12.
Pubmed: (View Article at PubMed) PMID:20549303
DOI: Full-text: DOI:10.1007/s11060-010-0237-2

Various antidepressants, mainly tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs), have exhibited potent anticancer properties in different cancer cell types. In the present study, desipramine (DMI), a representative of TCAs, was examined with respect to its apoptosis-inducing activity in rat C6 glioma cells and the underlying mechanism of action. DMI induced typical apoptotic morphology of chromatin condensation in rat glioma C6 cells and activated intracellular caspase 9 and caspase 3 with no change in mitochondrial membrane potential. Simultaneously, DMI significantly elevated expression of endoplasmic reticulum stress regulator CHOP/GADD153 and its targeting molecule GADD34. However, knockdown of CHOP by CHOP-specific short interfering RNA (siRNA) could decrease the activity of intracellular caspase 3 and the cytotoxicity of DMI to C6 cells. These results revealed that the CHOP-dependent endoplasmic reticulum (ER) stress pathway is responsible for DMI-induced apoptosis in C6 cells.


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CRRD Object Information
CRRD ID: 9999406
Created: 2015-04-17
Species: All species
Last Modified: 2015-04-17
Status: ACTIVE


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