1999年9月
Cripto-1 induces phosphatidylinositol 3 '-kinase-dependent phosphorylation of AKT and glycogen synthase kinase 3 beta in human cervical carcinoma cells
CANCER RESEARCH
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- 巻
- 59
- 号
- 18
- 開始ページ
- 4502
- 終了ページ
- 4505
- 記述言語
- 英語
- 掲載種別
- 出版者・発行元
- AMER ASSOC CANCER RESEARCH
Cripto-1 (CR-1), a member of the epidermal growth factor-CFC peptide family, activates the ras/raf/mitogen-activated protein/extracellular signal-regulated kinase/mitogen-activated protein kinase pathway. In the present study, the role of CR-1 in the phosphatidylinositol 3'-kinase (PI3K)/AKT (protein kinase B)/glycogen synthase kinase 3 beta (GSK-3 beta)dependent signaling pathway was evaluated in human SiHa cervical carcinoma cells. Our data demonstrate that CR-1 can enhance the tyrosine phosphorylation of the p85 regulatory subunit of PI3K and transiently induce the phosphorylation of AKT in a time- and dose-dependent manner. In addition, CR-1 was found to induce the phosphorylation of GSK-3 beta. Phosphorylation of AKT and GSK-3 beta by CR-1 can be blocked by LY294002, a specific inhibitor of PI3K;, thus leading to apoptosis. Finally, the apoptotic effect of LY294002 can be partially rescued by exogenous CR-1. In summary, our data suggest that human CR-1 may function as a survival factor through a PI3K-dependent signaling pathway involving AKT and GSK-3 beta.
- リンク情報
- ID情報
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- ISSN : 0008-5472
- Web of Science ID : WOS:000082541600003