Naphthoquinone analog-induced g1 arrest is mediated by cdc25A inhibition and p53-independent p21 induction in human hepatocarcinoma cells
김원호, 김정웅, 장상민, 송기현, 함승욱, 최경희,
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김원호 ( Kim Won-Ho ) - Chung-Ang University Department of Biology
김정웅 ( Kim Jung-Woong ) - Chung-Ang University Department of Biology
장상민 ( Jang Sang-Min ) - Chung-Ang University Department of Biology
송기현 ( Song Ki-Hyun ) - Chung-Ang University Department of Biology
함승욱 ( Ham Seung-Wook ) - Chung-Ang University Department of Chemistry
최경희 ( Choi Kyung-Hee ) - Chung-Ang University Department of Biology
Abstract
The naphthoquinone analog (2,3?dichloro?6,9?dihydroxy?1,4?naphtoquinone, NA) has an inhibitory effect on cdc25A protein phosphatase in vitro, which is responsible for G1/S transition during cell cycle. However, the exact mechanism inducing the growth inhibition is not understood. In this study, we investigated the regulatory mechanisms of growth arrest induced by NA, as a new potent inhibitor of cdc25A phosphatase, in human hepatocarcinoma SK?hep?1 cells. We found that NA induced the G1 arrest by perturbation of protein tyrosine dephosphorylation of Cdk2, which may be resulting from inhibition of cdc25A phosphatase. In addition, p21 was expressed in a p53?independent manner and participated in the NA?induced G1 arrest by inhibiting Cdk2 activity. Although the exact mechanism is not known, the p21 expression might be related to MAPK activation. From these results, we suggest that NA induces G1 arrest via inhibition of cdc25A and induction of p53?independent p21 expression in SK?Hep?1 cells.
키워드
Naphthoquinone analog (NA); G1 arrest; p53-independent p21; MAPK
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