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Growth Inhibition and Apoptosis of Neuroblastoma Cells Through ROS-Independent MEK/ERK Activation by Sulforaphane

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Abstract

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).

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Acknowledgments

We would like to express our appreciation for the financial support provided by Sin-Lau Hospital of Tainan (100-03 and 101-01).

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The authors declare no conflicts of interest.

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Correspondence to Yi-Chiang Hsu or Tzuu-Yuan Huang.

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Hsu, YC., Chang, SJ., Wang, MY. et al. Growth Inhibition and Apoptosis of Neuroblastoma Cells Through ROS-Independent MEK/ERK Activation by Sulforaphane. Cell Biochem Biophys 66, 765–774 (2013). https://doi.org/10.1007/s12013-013-9522-y

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