Growth Inhibition and Apoptosis of Neuroblastoma Cells Through ROS-Independent MEK/ERK Activation by Sulforaphane
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- 作者：Yi-Chiang Hsu (1) (2)
Sue-Joan Chang (3)
Miin-Yau Wang (2)
Yi-Ling Chen (2)
Tzuu-Yuan Huang (4) - 关键词：Sulforaphane ; Neuroblastoma ; Apoptosis ; ROS
- 刊名：Cell Biochemistry and Biophysics
- 出版年：2013
- 出版时间：July 2013
- 年：2013
- 卷：66
- 期：3
- 页码：765-774
- 全文大小：973KB
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Sue-Joan Chang (3)
Miin-Yau Wang (2)
Yi-Ling Chen (2)
Tzuu-Yuan Huang (4)
1. Graduate Institute of Medical Science, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan
2. Innovative Research Center of Medicine, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan
3. Department of Life Sciences, National Cheng Kung University, Tainan, Taiwan
4. Departments of Neurosurgery, Tainan Sin-Lau Hospital, Tainan, Taiwan
文摘
Deregulation of apoptosis alters the balance of cell proliferation and cell death, resulting in a variety of diseases, including cancer. In recent studies, sulforaphane (SFN) has demonstrated potent anti-tumor and chemopreventive activities. A possible signal transduction pathway has also been elucidated for SFN-induced apoptosis in human neuroblastoma SH-SY5Y cells. The present study further investigates the anti-proliferation activities of SFN through induced apoptosis in SH-SY5Y cells. We found that treating SH-SY5Y cells with SFN resulted in the depletion of mitochondrial membrane potential (Δψ), which in turn increased caspase 9, caspase 3, and the up-regulation of phosphorylated MEK/ERK without generating reactive oxygen species. Results were confirmed by MTT assay, which demonstrated the cytotoxic activity of SFN against SH-SY5Y cells (IC50 values of 20?μM).