PMID: 9533766Apr 9, 1998Paper

2-Deoxyglucose inhibits chemotherapeutic drug-induced apoptosis in human monocytic leukemia U937 cells with inhibition of c-Jun N-terminal kinase 1/stress-activated protein kinase activation

International Journal of Cancer. Journal International Du Cancer
N HagaT Tsuruo

Abstract

Human monocytic leukemia U937 cells undergo apoptosis when treated with antitumor drugs, such as etoposide, camptothecin and mitomycin C. The molecular mechanism of the drug-induced apoptosis is not well understood. In this study, we found that 2-deoxyglucose (2DG), an analog of D-glucose and an inducer of glucose-regulated stress, inhibited anticancer drug-induced but not tumor necrosis factor-alpha-induced apoptosis of U937 cells. 2DG did not reduce initial cellular damage caused by etoposide, an inhibitor of topoisomerase II, suggesting that 2DG affected subsequent cellular responses involved in apoptosis. 2DG inhibited the etoposide-induced activation of c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK) and the subsequent activation of CPP32, both of which are positive regulators for etoposide-induced apoptosis of U937 cells. Our results indicate that 2DG inhibits apoptosis by blocking the signals from cellular DNA damage for JNK1/SAPK activation.

References

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Nov 4, 1996·International Journal of Cancer. Journal International Du Cancer·A TomidaT Tsuruo

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Citations

Oct 26, 2000·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·D CrenesseA Schmid-Alliana
Mar 16, 2007·International Journal of Radiation Biology·A J HunterM J Renan
Aug 24, 2006·Apoptosis : an International Journal on Programmed Cell Death·Alistair HunterRaymond Abratt
Oct 26, 2010·Oncogene·N El MjiyadC Muñoz-Pinedo

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