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pubmed-article:16792413pubmed:abstractTextThe present study has demonstrated a differential cytotoxicity of stellettin A (1) between human leukemia HL-60 cells (IC50 0.4 microg/mL) and human prostate cancer LNCaP cells (IC50 120 microg/mL). Treatment of cells with 1 revealed the activation of NADPH oxidase, the dramatic generation of reactive oxygen species, and the dissipation of mitochondrial membrane potentials, with HL-60 cells being more sensitive than LNCaP cells by an order of magnitude. Immunoblotting analysis further demonstrated a stronger upregulation of the apoptosis marker proteins, FasL and caspase-3, in HL-60 cells, and pretreatment of cells with antisense oligonucleotide for caspase-3 abolished apoptosis. All available evidence suggests that 1 induces oxidative cell death through a FasL-caspase-3-apoptotic pathway.lld:pubmed
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pubmed-article:16792413pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:16792413pubmed:articleTitleStellettin A induces oxidative stress and apoptosis in HL-60 human leukemia and LNCaP prostate cancer cell lines.lld:pubmed
pubmed-article:16792413pubmed:affiliationDepartment of Anatomy and School of Chinese Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, People's Republic of China. ken-liu@cuhk.edu.hklld:pubmed
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