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Title 

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

Authors 

E M LeeH R ParkJ H HwangDong Jin parkK S ChangChang-Jin Kim

Publisher 

The Korean Society for Applied Microbiology

Issue Date 

2007

Citation 

Journal of Microbiology and Biotechnology, vol. 17, no. 11, pp. 1856-1861

Keywords 

anticanceretoposide resistanceglucose deprivationmithramycinsolid tumoretoposideglucosecancer resistancecarcinoma cellcell strain HT29

Abstract 

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.

ISSN 

1017-7825

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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