Journal of Microbiology and Biotechnology

  • 제17권11호
  • /
  • Pages.1856-1861
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  • 2007
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  • 1017-7825(pISSN)
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  • 1738-8872(eISSN)
한국미생물·생명공학회 (The Korean Society for Microbiology and Biotechnology)
권호 표지

Mithramycin Inhibits Etoposide Resistance in Glucose-deprived HT-29 Human Colon Carcinoma Cells

  • Lee, Eun-Mi (Korea Research Institute of Bioscience and Biotechnology) ;
  • Park, Hae-Ryong (Department of Food Science and Biotechnology, Kyungnam University) ;
  • Hwang, Ji-Hwan (Department of Food Science and Biotechnology, Kyungnam University) ;
  • Park, Dong-Jin (Korea Research Institute of Bioscience and Biotechnology) ;
  • Chang, Kyu-Seob (Department of Food Science and Technology, Chungnam National University) ;
  • Kim, Chang-Jin (Korea Research Institute of Bioscience and Biotechnology)
  • 발행 : 2007.11.30
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초록

Physiological cell conditions such as glucose deprivation and hypoxia play roles in the development of drug resistance in solid tumors. These tumor-specific conditions cause decreased expression of DNA topoisomerase $II{\alpha}$, rendering cells resistant to topo II target drugs such as etoposide. Thus, targeting tumor-specific conditions such as a low glucose environment may be a novel strategy in the development of anticancer drugs. On this basis, we established a novel screening program for anticancer agents with preferential cytotoxic activity in cancer cells under glucose-deprived conditions. We recently isolated an active compound, AA-98, from Streptomyces sp. AA030098 that can prevent stress-induced etoposide resistance in vitro. Furthermore, LC-MS and various NMR spectroscopic methods identified AA-98 as mithramycin, which belongs to the aureolic acid group of antitumor compounds. We found that mithramycin prevents the etoposide resistance that is induced by glucose deprivation. The etoposide-chemosensitive action of mithramycin was just dependent on strict low glucose conditions, and resulted in the selective cell death of etoposide-resistant HT-29 human colon cancer cells.

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