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저자정보
Kim, Joo-Hwan (Department of Toxicological Researches, National Institute of Toxicological Research, Korea Food and Drug Administration) Koo, Ye-Mo (Department of Toxicological Researches, National Institute of Toxicological Research, Korea Food and Drug Administration) Lee, Woo-Sun (Department of Toxicological Researches, National Institute of Toxicological Research, Korea Food and Drug Administration) Suh, Soo-Kyung (Department of Toxicological Researches, National Institute of Toxicological Research, Korea Food and Drug Administration) Kang, Jin-Seok (Department of Toxicological Researches, National Institute of Toxicological Research, Korea Food and Drug Administration) Han, Eui-Sik (Department of Toxicological Researches, National Institute of Toxicological Research, Korea Food and Drug Administration) Kim, Seung-Hee (Department of Toxicological Researches, National Institute of Toxicological Research, Korea Food and Drug Administration) Park, Sue-N. (Department of Toxicological Researches, National Institute of Toxicological Research, Korea Food and Drug Administration)
저널정보
대한독성유전단백체학회 Molecular & cellular toxicology Molecular & cellular toxicology 제3권 제3호
발행연도
2007.1
수록면
165 - 171 (7page)

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Mitomycin C (MMC), an antitumor antibiotic isolated from Streptomyces caespitosus, is used in chemotherapy of gastric, bladder and colorectal cancer. MMC is activated in vivo to alkylate and crosslink DNA, via G-G interstrand bonds, thereby inhibiting DNA synthesis and transcription. This study investigates gene expression changes in response to MMC treatment in order to elucidate the mechanisms of MMC-induced toxicity. MMC was admistered with single dose (0.32 and 1.6 ${\mu}M$) to TK6 cells. Applied Biosystem's DNA chips were used for identifying the gene expression profile by MMC-induced toxicity. We identified up- or down-regulated 90 genes including cyclin M2, cyclin-dependent kinase inhibitor 1A (p21, cip1), programmed cell death 1, tumor necrosis factor (ligand) superfamily, member 9, et al. The regulated genes by MMC associated with the biological pathways apoptosis signaling pathway. Further characterization of these candidate markers related to the toxicity will be useful to understand the detailed mechanism of action of MMC.

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