NDLI: Kaempferol Induces Cell Death Through ERK and Akt-Dependent Down-Regulation of XIAP and Survivin in Human Glioma Cells

Content Provider	Springer Nature Link
Author	Jeong, Ji Cheon Kim, Min Soo Kim, Thae Hyun Kim, Yong Keun
Copyright Year	2008
Abstract	The present study was undertaken to determine the molecular mechanism by which kaempferol induces cell death in human glioma cells. Kaempferol resulted in loss of cell viability and inhibition of proliferation in a dose- and time-dependent manner, which were largely attributed to cell death. Kaempferol caused an increase in reactive oxygen species (ROS) generation and the kaempferol-induced cell death was prevented by antioxidants, suggesting that ROS generation is involved in kaempferol-induced cell death. Kaempferol caused depolarization of mitochondrial membrane potential. Western blot analysis showed that kaempferol treatment caused a rapid reduction in phosphorylation of extracellular signal-regulated kinase (ERK) and Akt. The ERK inhibitor U0126 and the Akt inhibitor LY984002 increased the kaempferol-induced cell death and overexpression of MEK, the upstream kinase of ERK, and Akt prevented the cell death. The expression of anti-apoptotic proteins XIAP and survivin was down-regulated by kaempferol and its effect was prevented by overexpression of MEK and Akt. Kaempferol induced activation of caspase-3 and kaempferol-induced cell death was prevented by caspase inhibitors. Taken together, these findings suggest that kaempferol results in human glioma cell death through caspase-dependent mechanisms involving down-regulation of XIAP and survivin regulating by ERK and Akt.
Starting Page	991
Ending Page	1001
Page Count	11
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	34
Issue Number	5
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2008-10-24
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Kaempferol Cell viability ERK Akt XIAP Survivin Human glioma cells Neurology Biochemistry Neurosciences
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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