Transcriptional upregulation of BAG3 upon proteasome inhibition
- Department of Anesthesiology, the 1st Affiliated Hospital, China Medical University, Shenyang 110001 (China)
- Department of Geriatrics, the 1st Affiliated Hospital, China Medical University, Shenyang 110001 (China)
- Department of Biochemistry and Molecular Biology, China Medical University, Shenyang 110001 (China)
- Department of Endocrinology and Metabolism, the 1st Affiliated Hospital, China Medical University, Shenyang 110001 (China)
Proteasome inhibitors exhibit antitumoral activity against malignancies of different histology. Emerging evidence indicates that antiapoptotic factors may also accumulate as a consequence of exposure to these drugs, thus it seems plausible that activation of survival signaling cascades might compromise their antitumoral effects. Bcl-2-associated athanogene (BAG) family proteins are characterized by their property of interaction with a variety of partners involved in modulating the proliferation/death balance, including heat shock proteins (HSP), Bcl-2, Raf-1. In this report, we demonstrated that BAG3 is a novel antiapoptotic molecule induced by proteasome inhibitors in various cancer cells at the transcriptional level. Moreover, we demonstrated that BAG3 knockdown by siRNA sensitized cancer cells to MG132-induced apoptosis. Taken together, our results suggest that BAG3 induction might represents as an unwanted molecular consequence of utilizing proteasome inhibitors to combat tumors.
- OSTI ID:
- 21043577
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 365, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2007.11.001; PII: S0006-291X(07)02383-2; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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