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Carcinogenesis Advance Access published online on June 19, 2003
Carcinogenesis, doi:10.1093/carcin/bgg097
© 2003 by Oxford University Press
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© 2003 Oxford University Press

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Panaxadiol selectively inhibits Cyclin A-associated Cdk2 activity by elevating p21WAF1/CIP1 protein levels in mammalian cells

Ying Hua Jin 1, JoonSeok Choi 2, Soona Shin 2, KwangYoul Lee 3, Jeong Hill Park 4, and Seung Ki Lee 1*

1 Division of Pharmaceutical Biosciences, College of Pharmacy, Seoul National University, Seoul 151-742, South Korea; The Research Institute for Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 151-742, South Korea
2 Division of Pharmaceutical Biosciences, College of Pharmacy, Seoul National University, Seoul 151-742, South Korea
3 Department of Biochemistry, College of Medicine, Institute of Medical Research, Chungbuk National University, Cheongju, 361-763, South Korea
4 The Research Institute for Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 151-742, South Korea

* Corresponding author. E-mail: sklcrs{at}plaza.snu.ac.kr.

Received 6 January 2003 ; revised 1 May 2003 ; accepted 28 May 2003

Abstract

We show that panaxadiol (PD), a ginseng saponin with a dammarane skeleton, selectively interferes with the cell cycle in human cancer cell lines. PD inhibited DNA synthesis in a dose-dependent manner with IC50 values ranging from 0.8 µM-1.2 µM in SK-HEP-1 cells and HeLa cells. PD-treated cells were arrested at G1/S phase, which coincided well with decreases in Cyclin A-Cdk2 activity, but not in Cyclin E-Cdk2 and Cdc2 activities. The intracellular levels of p21WAF1/CIP1 were significantly and selectively elevated in a dose- and time-dependent manners in PD-treated HeLa cells. Similarly, levels of the p21WAF1/CIP1 protein that is associated with the Cyclin A-Cdk2 complex increased, and these increases correlated well with the down-regulation of Cyclin A-Cdk2 activity. Thus, PD selectively elevates p21WAF1/CIP1 levels and thereby arrests the cell cycle at G1/S phase by down-regulating Cyclin A-Cdk2 activity.


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