摘要：

Menadione (2-methyl-1,4-naphthoquinone, or vitamin K3), a synthetic congener of naturally occurring vitamin K1 and K2, has increasingly been of interest given its broad range of antitumor activity in human cells. Although oxidative stress was a common mechanism of tumor growth inhibition by menadione, it was reported in 1993 by Juan and Wu that menadione induces alterations in the phosphorylation status of p34~(cdc2) kinase (cdkl) and the activity of protein tyrosine phosphatases (PTPases) during cell cycle progression. On the basis of this result, this lab demonstrated that menadione is an inactivator of cdc25 phosphatase because cdc25 phosphatase dephosphorylates cdk at the Thr-14 and Tyr-15 residues and thus stimulates cdk activity. Since then, another possible mechanism of menadione cytotoxicity has been ascribed to inactivation of cdc25 phosphatases.

展开