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2‐(4‐methylphenyl)‐1,3‐selenazol‐4‐one induces apoptosis by different mechanisms in SKOV3 and HL 60 cells
Author(s) -
Ahn Hak Jun,
Koketsu Mamoru,
Yang Eun Mi,
Kim Yong Man,
Ishihara Hideharu,
Yang Hyun Ok
Publication year - 2006
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20973
Subject(s) - apoptosis , dna fragmentation , microbiology and biotechnology , cell culture , flow cytometry , chemistry , cell , cell cycle , biology , programmed cell death , biochemistry , genetics
We examined the ability of the synthetic selenium compound, 2‐(4‐methylphenyl)‐1,3‐selenazol‐4‐one (hereafter designated 3a ), to induce apoptosis in a human ovarian cancer cell line (SKOV3) and a human leukemia cell line (HL‐60). Flow cytometry showed that 3a treatment induced apoptosis in both cell lines to degrees comparable to that of the positive control, paclitaxel. Apoptosis was measured by PS externalization, DNA fragmentation and decreased mitochondrial membrane potential (MMP). However, analysis of the mechanism of action revealed differences between the responses of the two cell lines. Treatment with 3a arrested the cell cycle and induced caspase‐3 activation in HL‐60 cells, but not in SKOV3 cells. In contrast, 3a treatment induced apoptosis through translocation of AIF, a novel pro‐apoptotic protein, in SKOV3 cells, but not in HL‐60 cells. Collectively, our data demonstrated that 3a induced apoptosis in both cell lines, but via different action mechanisms. J. Cell. Biochem. 99: 807–815, 2006. © 2006 Wiley‐Liss, Inc.