Transcriptional and post-translational regulation of Bim controls apoptosis in melatonin-treated human renal cancer Caki cells

Authors
Eun Jung ParkSeon Min WooKyoung-jin MinTaeg Kyu Kwon
Department
Dept. of Immunology (면역학)
Issue Date
2014
Citation
Journal of Pineal Research, Vol.56(1) : 97-106, 2014
ISSN
0742-3098
Abstract
Melatonin (N-acetyl-5-methoxytryptamine) has recently gained attention as an anticancer agent and for combined cancer therapy. In this study, we investigated the underlying molecular mechanisms of the effects of melatonin on cancer cell death. Treatment with melatonin induced apoptosis and upregulated the expression of the pro-apoptotic protein Bcl-2-interacting mediator of cell death (Bim) in renal cancer Caki cells. Furthermore, downregulation of Bim expression by siRNA markedly reduced melatonin-mediated apoptosis. Melatonin increased Bim mRNA expression through the induction of Sp1 and E2F1 expression and transcriptional activity. We found that melatonin also modulated Bim protein stability through the inhibition of proteasome activity. However, melatonin-induced Bim upregulation was independent of melatonin's antioxidant properties and the melatonin receptor. Taken together, our results suggest that melatonin induces apoptosis through the upregulation of Bim expression at the transcriptional level and at the post-translational level.
Keywords
apoptosisBimmelatoninproteasome activitytranscriptional regulation
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/34240
Appears in Collections:
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
Keimyung Author(s)
권택규
Full Text
http://lps3.onlinelibrary.wiley.com.proxy.dsmc.or.kr/doi/abs/10.1111/jpi.12102
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