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Title 

Doxorubicin prevents endoplasmic reticulum stress-induced apoptosis

Authors 

Soo Jung KimKyung Mi ParkNaYoung KimYoung Il Yeom

Publisher 

Elsevier

Issue Date 

2006

Citation 

Biochemical and Biophysical Research Communications, vol. 339, no. 2, pp. 463-468

Keywords 

apoptosisdoxorubicinstress signalingthapsigarginunfolded protein response3' (3 cyanomorpholino) 3' deaminodoxorubicinendoplasmic reticulumstress

Abstract 

Several cellular stress signaling pathways initiate apoptosis in eukaryotic cells, but the interactions and coordination between the pathways have not been elucidated. In this study, apoptosis was triggered in MCF7 human breast carcinoma cells using doxorubicin, a topoisomerase inhibitor, and an endoplasmic reticulum (ER) stress inducer, thapsigargin, the latter causing the unfolded protein response (UPR). Interestingly, compared to treatment with doxorubicin or thapsigargin alone, cell death was reduced by treatment with both stress inducers. In contrast to another topoisomerase inhibitor, etoposide, doxorubicin markedly decreased apoptosis induced by thapsigargin; this doxorubicin effect was accompanied by reduced expression of the UPR-specific proapoptotic protein, C/EBP-homologous protein, and its upstream transcription factor, ATF4. We further found that doxorubicin downregulates the expression of ATF4 mRNA, indicating that doxorubicin interferes with the UPR at the level of ATF4 transcription. Taken together, the data suggest that ER stress-initiated cell death might be regulated by doxorubicin.

ISSN 

0006-291X

Link 

http://dx.doi.org/10.1016/j.bbrc.2005.11.040

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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