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Environ Toxicol. 2017 Jan;32(1):311-328. doi: 10.1002/tox.22237. Epub 2016 Feb 2.

Sulforaphane-induced apoptosis in human leukemia HL-60 cells through extrinsic and intrinsic signal pathways and altering associated genes expression assayed by cDNA microarray.

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Department of Pathology, National Defense Medical Center, Division of Clinical Pathology, Tri-Service General Hospital, Taipei, Taiwan.
School of Medicine, Fu-Jen Catholic University, Taipei, Taiwan.
Department of Pathology and Laboratory Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
School of Medical Laboratory Science and Biotechnology, Taipei Medical University, Taipei, Taiwan.
Jen-the Junior College of Medicine, Nursing and Management, Miaoli County, Taiwan.
Departments of Clinical Pathology, Cheng Hsin General Hospital, Taipei, Taiwan.
Department of Medical Laboratory Science and Biotechnology, Yuanpei University, Hsinchu, Taiwan.
Department of Physiology, China Medical University, Taichung 404, Taiwan.
Departments of Restaurant, Hotel and Institutional Management, Fu-Jen Catholic University, Taipei, Taiwan.
Department of Biological Science and Technology, China Medical University, Taichung, Taiwan.
Department of Biotechnology, Asia University, Taichung, Taiwan.


Sulforaphane (SFN), one of the isothiocyanates, is a biologically active compound extracted from cruciferous vegetables, and has been shown to induce cytotoxic effects on many human cancer cells including human leukemia cells. However, the exact molecular mechanism and altered gene expression associated with apoptosis is unclear. In this study, we investigated SFN-induced cytotoxic effects and whether or not they went through cell-cycle arrest and induction of apoptosis and further examined molecular mechanism and altered gene expression in human leukemia HL-60 cells. Cell viability, cell-cycle distribution, sub-G1 (apoptosis), reactive oxygen species (ROS) and Ca2+ production, levels of mitochondrial membrane potential (ΔΨm ), and caspase-3, -8, and -9 activities were assayed by flow cytometry. Apoptosis-associated proteins levels and gene expressions were examined by Western blotting and cDNA microarray assays, respectively. Results indicated that SFN decreased viable cells, induced G2/M phase arrest and apoptosis based on sub-G1 phase development. Furthermore, SFN increased ROS and Ca2+ production and decreased the levels of ΔΨm and activated caspase-3, -8, and -9 activities in HL-60 cells. SFN significantly upregulated the expression of BAX, Bid, Fas, Fas-L, caspase-8, Endo G, AIF, and cytochrome c, and inhibited the antiapoptotic proteins such as Bcl-x and XIAP, that is associated with apoptosis. We also used cDNA microarray to confirm several gene expressions such as caspase -8, -3, -4, -6, and -7 that are affected by SFN. Those results indicated that SFN induced apoptosis in HL-60 cells via Fas- and mitochondria-dependent pathways.


apoptosis; cDNA microarray; human leukemia HL-60 cells; sulforaphane

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