Mithramycin inhibits etoposide resistance in glucose-deprived HT-29 human colon carcinoma cells

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Mithramycin inhibits etoposide resistance in glucose-deprived HT-29 human colon carcinoma cells
E M Lee; H R Park; J H Hwang; Dong Jin park; K S Chang; Chang-Jin Kim
Bibliographic Citation
Journal of Microbiology and Biotechnology, vol. 17, no. 11, pp. 1856-1861
Publication Year
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 IIα, 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.
anticanceretoposide resistanceglucose deprivationmithramycinsolid tumor
Korea Soc-Assoc-Inst
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Division of Biomedical Research > Microbiome Convergence Research Center > 1. Journal Articles
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