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엄지현,강치덕,배재호,신진구,김도완,김동완,정병선,김선희 생화학분자생물학회 2004 Experimental and molecular medicine Vol.36 No.3
Tumor hypoxia contributes to the progression of a malignant phenotype and resistance to ioniz-ing radiation and anticancer drug therapy. Many mediated by expression of specific set of genes whose relation to therapy resistance is porly understod. In this study, we revealed that DNA-dependent protein kinase (DNA-PK), which plays a crucial role in DNA double strand break repair, would be involved in regulation of hypoxia inducible factor-1 (HIF-1). HIF-1β-defi-cient cells showed constitutively reduced ex-presion and DNA-binding activity of Ku, the regulatory subunit of DNA-PK. Under hypoxic condition, the expresion and activity of DNA- increase in HIF-1α expresion. Our result also demonstrated that DNA-PK could directly in-teract with HIF-1, and especially DNA-PKcs, the catalytic subunit of DNA-PK, could be involved in phosphorylation of HIF-1α, suggesting the posibility that the enhanced expresion of DNA- PK under hypoxic condition might atribute to modulate HIF-1α stabilization. Thus, the corel-ated regulation of DNA-PK with HIF-1 could cells, and it provides new evidence for developing therapeutic strategies enhancing the efficacy of cancer therapy in hypoxic tumor cells.