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PTEN modulates cell cycle progression and cell survival by regulating phosphatidylinositol 3,4,5,-trisphosphate and Akt/protein kinase B signaling pathway
Open accessAbstract
To investigate the molecular basis of PTEN-mediated tumor suppression, we introduced a null mutation into the mouse Pten gene by homologous recombination in embryonic stem (ES) cells. Pten −/− ES cells exhibited an increased growth rate and proliferated even in the absence of serum. ES cells lacking PTEN function also displayed advanced entry into S phase. This accelerated G 1 /S transition was accompanied by down-regulation of p27 KIP1 , a major inhibitor for G 1 cyclin-dependent kinases. Inactivation of PTEN in ES cells and in embryonic fibroblasts resulted in elevated levels of phosphatidylinositol 3,4,5,-trisphosphate, a product of phosphatidylinositol 3 kinase. Consequently, PTEN deficiency led to dosage-dependent increases in phosphorylation and activation of Akt/protein kinase B, a well-characterized target of the phosphatidylinositol 3 kinase signaling pathway. Akt activation increased Bad phosphorylation and promoted Pten −/− cell survival. Our studies suggest that PTEN regulates the phosphatidylinositol 3,4,5,-trisphosphate and Akt signaling pathway and consequently modulates two critical cellular processes: cell cycle progression and cell survival.
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Metadata
- Authors
- Sun, H., Lesche, R., Li, D.-M., Liliental, J., Zhang, H., Gao, J., Gavrilova, N., Mueller, B., Liu, X., & Wu, H.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-05-25
- Volume
- 96
- Issue
- 11
- Pages
- 6199-6204
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2111125738
- Cited by
- 796
- References
- 2
- FWCI
- 15.55
- Type
- journal article
- Language
- en
- Open access
- green
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