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).
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Anticarcinogenic Agents / pharmacology*
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Apoptosis / drug effects*
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Carcinogenesis / drug effects
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Caspase 3 / metabolism
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Caspase 9 / metabolism
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Cell Line, Tumor
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Cell Movement / drug effects
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Cell Proliferation / drug effects
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Cell Survival / drug effects
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Enzyme Activation / drug effects
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Extracellular Signal-Regulated MAP Kinases / metabolism*
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G1 Phase / drug effects
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Humans
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Isothiocyanates / pharmacology*
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MAP Kinase Signaling System / drug effects
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Membrane Potential, Mitochondrial / drug effects
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Mitogen-Activated Protein Kinase Kinases / metabolism*
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Neoplasm Invasiveness
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Neuroblastoma / pathology*
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Reactive Oxygen Species / metabolism
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Sulfoxides
Substances
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Anticarcinogenic Agents
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Isothiocyanates
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Reactive Oxygen Species
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Sulfoxides
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Extracellular Signal-Regulated MAP Kinases
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Mitogen-Activated Protein Kinase Kinases
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Caspase 3
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Caspase 9
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sulforaphane