Abstract |
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.
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Authors | Hak Jun Ahn, Mamoru Koketsu, Eun Mi Yang, Yong Man Kim, Hideharu Ishihara, Hyun Ok Yang |
Journal | Journal of cellular biochemistry
(J Cell Biochem)
Vol. 99
Issue 3
Pg. 807-15
(Oct 15 2006)
ISSN: 0730-2312 [Print] United States |
PMID | 16676363
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | 2006 Wiley-Liss, Inc. |
Chemical References |
- 2-(4-Methylphenyl)-1,3-selenazol-4-one
- Antineoplastic Agents
- Apoptosis Inducing Factor
- Azoles
- Organoselenium Compounds
- Caspase 3
- Paclitaxel
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Topics |
- Animals
- Antineoplastic Agents
(pharmacology)
- Apoptosis
(drug effects)
- Apoptosis Inducing Factor
(metabolism)
- Azoles
(pharmacology)
- Caspase 3
(metabolism)
- Cell Cycle
(drug effects)
- Cell Line, Tumor
(drug effects)
- Cell Nucleus
(metabolism)
- DNA Fragmentation
- Enzyme Activation
- Humans
- Membrane Potentials
(physiology)
- Mitochondria
(metabolism)
- Organoselenium Compounds
(pharmacology)
- Paclitaxel
(pharmacology)
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