Abstract | BACKGROUND: MATERIALS AND METHODS: H9 and Raji lymphoma cells were grown in culture and exposed to imexon, radiation, or both. Cells were assessed for cell viability, glutathione content, induction of apoptosis, cell cycle distribution and also subject to Western blot analysis. RESULTS:
Imexon inhibited cell proliferation in a dose-dependent manner. Imexon, given for 48 h prior to irradiation at a clinically achievable dose of 40 muM, potently enhanced the cell radiosensitivity. Imexon enhanced radiation-induced apoptosis and accumulated cells in G2/M phase of the cell cycle. Imexon induced caspase-3 activation and PARP cleavage. Alterations in glutathione levels were not observed at 40 microM of imexon. CONCLUSION: In conclusion, imexon efficiently augmented lymphoma cell radiosensitivity independently of glutathione and the underlying mechanisms include induction of apoptosis and cell cycle redistribution.
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Authors | Heunglae Cho, Masashi Koto, Oliver Riesterer, David P Molkentine, Uma Giri, Luka Milas, Michael D Story, Chul S Ha, Uma Raju |
Journal | Anticancer research
(Anticancer Res)
Vol. 29
Issue 11
Pg. 4409-15
(Nov 2009)
ISSN: 1791-7530 [Electronic] Greece |
PMID | 20032386
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Hexanones
- Radiation-Sensitizing Agents
- 4-imino-1,3-diazabicyclo(3.1.0)hexan-2-one
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Topics |
- Apoptosis
(drug effects)
- Blotting, Western
- Cell Cycle
(drug effects)
- Cell Line, Tumor
- Combined Modality Therapy
- Hexanones
(pharmacology)
- Humans
- Lymphoma, Non-Hodgkin
(drug therapy, metabolism, pathology, radiotherapy)
- Lymphoma, T-Cell
(drug therapy, metabolism, pathology, radiotherapy)
- Oxidation-Reduction
- Radiation-Sensitizing Agents
(pharmacology)
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