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논문 기본 정보
- 자료유형
- 학술대회자료
- 저자정보
- 발행연도
- 2006.5
- 수록면
- 3 - 12 (10page)
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초록· 키워드
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1 The present work was performed to investigate the effects of ginsenoside Rh2 on proliferation, cell cycle-regulation and differentiation of human leukemia HL-60 cells as well as the underlying mechanisms for these effects.
2 Ginsenoside Rh2 potently inhibited the proliferation of HL-60 cells in both a dose- and timedependent manner with an IC??, 20 μM.
3 DNA flow-cytometry indicated that ginsenoside Rh2 markedly induced a G1 phase arrest of HL-60 cells.
4 Among the G1 phase cell cycle-related proteins, the levels of cyclin-dependent kinase (CDK)4, 6 and cyclin D1, cyclin D2, cyclin D3 were reduced by ginsenoside Rh2, whereas the steadystate levels of CDK2 and cyclin E were unaffected.
5 The protein levels of a CDK inhibitor p16, p21<SUP>CIP1/WAF1</SUP> and p27<SUP>KIP1</SUP> were markedly increased by ginsenoside Rh2.
6 Ginsenoside Rh2 markedly enhanced the binding of p21<SUP>CIP1/WAF1</SUP> and p27<SUP>KIP1</SUP> with CDK2 and CDK6, resulting in the reduced activity of both kinases and the hypophosphorylation of Rb protein.
7 We furthermore suggest that ginsenoside Rh2 is a potent inducer of the differentiation of HL-60 cells, based on observations such as a reduction of the nitroblue tetrazolium level, an increase in the esterase activities and phagocytic activity, morphology changes, and the expression of CD11b, CD14, CD64 and CD66b surface antigens.
8 In conclusion, the onset of ginsenoside Rh2-induced the G?/G₁ arrest of HL-60 cells prior to the differentiation is linked to a sharp up-regulation of the p21<SUP>CIP1/WAF1</SUP> level and a decrease in the CDK2, CDK4 and CDK6 activities. This is the first report demonstrating that ginsenoside Rh2 potently inhibits the proliferation of human promyelocytic HL-60 cells via the G1 phase cell cycle arrest and differentiation induction.
2 Ginsenoside Rh2 potently inhibited the proliferation of HL-60 cells in both a dose- and timedependent manner with an IC??, 20 μM.
3 DNA flow-cytometry indicated that ginsenoside Rh2 markedly induced a G1 phase arrest of HL-60 cells.
4 Among the G1 phase cell cycle-related proteins, the levels of cyclin-dependent kinase (CDK)4, 6 and cyclin D1, cyclin D2, cyclin D3 were reduced by ginsenoside Rh2, whereas the steadystate levels of CDK2 and cyclin E were unaffected.
5 The protein levels of a CDK inhibitor p16, p21<SUP>CIP1/WAF1</SUP> and p27<SUP>KIP1</SUP> were markedly increased by ginsenoside Rh2.
6 Ginsenoside Rh2 markedly enhanced the binding of p21<SUP>CIP1/WAF1</SUP> and p27<SUP>KIP1</SUP> with CDK2 and CDK6, resulting in the reduced activity of both kinases and the hypophosphorylation of Rb protein.
7 We furthermore suggest that ginsenoside Rh2 is a potent inducer of the differentiation of HL-60 cells, based on observations such as a reduction of the nitroblue tetrazolium level, an increase in the esterase activities and phagocytic activity, morphology changes, and the expression of CD11b, CD14, CD64 and CD66b surface antigens.
8 In conclusion, the onset of ginsenoside Rh2-induced the G?/G₁ arrest of HL-60 cells prior to the differentiation is linked to a sharp up-regulation of the p21<SUP>CIP1/WAF1</SUP> level and a decrease in the CDK2, CDK4 and CDK6 activities. This is the first report demonstrating that ginsenoside Rh2 potently inhibits the proliferation of human promyelocytic HL-60 cells via the G1 phase cell cycle arrest and differentiation induction.
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Summary
Introduction
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