Induction of G₁ cell cycle arrest and p27^KIP1 increase by panaxydol isolated from Panax ginseng

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• 作者：Moon ; Jungae ; Yu ; Su-Jin ; Kim ; Hyeon-Soo ; Sohn ; Jeongwon
• 关键词：panaxydol ; cell cycle ; G₁ arrest ; p27^KIP1 ; Cdk2 ; melanoma
• 刊名：Biochemical Pharmacology
• 出版年：2000
• 出版时间：May 1, 2000
• 年：2000
• 卷：59
• 期：9
• 页码：1109-1116
• 全文大小：666 K

文摘

Polyacetylenic compounds of Panax ginseng roots have been shown to inhibit growth of several human malignant tumor cell lines. Panaxydol is known to be one of the cytotoxic polyacetylenic compounds of P. ginseng. In this study, we first showed that panaxydol decreased markedly the proliferation, and to a lesser extent, the number of cells in a human melanoma cell line, SK-MEL-1. Next, the effect of panaxydol on cell cycle progression and its mechanism of action were investigated. Cell cycle analysis revealed that panaxydol inhibited cell cycle progression of a human malignant melanoma cell line, SK-MEL-1, at G₁-S transition. At the same time, panaxydol increased the protein expression of p27^KIP1 as early as 1 hr after treatment. Cyclin-dependent kinase 2 (Cdk2) activity was decreased in a dose-dependent manner after 24 hr of panaxydol treatment. Protein levels of p21^WAF1, p16^INK4a, p53, pRb (retinoblastoma protein), and E2F-1 were not changed. It was also found that cycloheximide reversed the growth inhibition induced by panaxydol and partially abrogated the increase in p27^KIP1 expression. These results indicate that panaxydol induces G₁ cell cycle arrest by decreasing Cdk2 activity and up-regulating p27^KIP1 protein expression.