Journal Article

Panaxadiol selectively inhibits cyclin A-associated Cdk2 activity by elevating p21<i><sup>WAF1/CIP1</sup></i> protein levels in mammalian cells

Ying Hua Jin, JoonSeok Choi, Soona Shin, Kwang Youl Lee, Jeong Hill Park and Seung Ki Lee

in Carcinogenesis

Volume 24, issue 11, pages 1767-1772
Published in print November 2003 | ISSN: 0143-3334
Published online November 2003 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgg097
Panaxadiol selectively inhibits cyclin A-associated Cdk2 activity by elevating p21WAF1/CIP1 protein levels in mammalian cells

More Like This

Show all results sharing this subject:

  • Clinical Cytogenetics and Molecular Genetics

GO

Show Summary Details

Preview

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 to 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 manner 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.

Keywords: CDK, cyclin-dependent kinase; Cyclin A–Cdk2, Cyclin A-dependent kinase 2; CKIs, Cyclin-dependent kinase inhibitors; DAPI, 4,6-diamidino-2-phenylindole; PD, panaxadiol

Journal Article.  3826 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.