Journal of Neuro-Oncology

, Volume 101, Issue 1, pp 41–48

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

Laboratory Investigation - Human/Animal Tissue

DOI: 10.1007/s11060-010-0237-2

Cite this article as:
Ma, J., Qiu, Y., Yang, L. et al. J Neurooncol (2011) 101: 41. 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.


Desipramine Apoptosis Endoplasmic reticulum stress CHOP/GADD153 GADD34 

Copyright information

© Springer Science+Business Media, LLC. 2010

Authors and Affiliations

  • Jian Ma
    • 1
  • Yu Qiu
    • 1
  • Lan Yang
    • 1
  • Liang Peng
    • 1
  • Zheng Xia
    • 1
  • Li-Na Hou
    • 1
  • Chao Fang
    • 1
  • Hong Qi
    • 1
  • Hong-Zhuan Chen
    • 1
  1. 1.Department of PharmacologyInstitute of Medical Sciences, Shanghai Jiao Tong University School of MedicineShanghaiChina

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