Essential Role of AKT-1/Protein Kinase Balpha in PTEN-Controlled Tumorigenesis Export

@article{citeulike:4847394, abstract = {PTEN is mutated at high frequency in many primary human cancers and several familial cancer predisposition disorders. Activation of AKT is a common event in tumors in which the PTEN gene has been inactivated. We previously showed that deletion of the murine Pten gene in embryonic stem (ES) cells led to increased phosphatidylinositol triphosphate (PIP3) accumulation, enhanced entry into S phase, and better cell survival. Since PIP3 controls multiple signaling molecules, it was not clear to what degree the observed phenotypes were due to deregulated AKT activity. In this study, we mutated Akt-1 in Pten-/- ES cells to directly assess the role of AKT-1 in PTEN-controlled cellular processes, such as cell proliferation, cell survival, and tumorigenesis in nude mice. We showed that AKT-1 is one of the major downstream effectors of PTEN in ES cells and that activation of AKT-1 is required for both the cell survival and cell proliferation phenotypes observed in Pten-/- ES cells. Deletion of Akt-1 partially reverses the aggressive growth of Pten-/- ES cells in vivo, suggesting that AKT-1 plays an essential role in PTEN-controlled tumorigenesis. 10.1128/MCB.22.11.3842-3851.2002}, author = {Stiles, Bangyan and Gilman, Valeriya and Khanzenzon, Natalya and Lesche, Ralf and Li, Annie and Qiao, Rong and Liu, Xin and Wu, Hong}, citeulike-article-id = {4847394}, citeulike-linkout-0 = {http://dx.doi.org/10.1128/MCB.22.11.3842-3851.2002}, citeulike-linkout-1 = {http://mcb.asm.org/cgi/content/abstract/22/11/3842}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/11997518}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=11997518}, day = {1}, doi = {10.1128/MCB.22.11.3842-3851.2002}, journal = {Mol. Cell. Biol.}, keywords = {akt, apoptosis, esc, pten}, month = {June}, number = {11}, pages = {3842--3851}, posted-at = {2009-06-14 18:38:24}, priority = {2}, title = {Essential Role of AKT-1/Protein Kinase B{alpha} in PTEN-Controlled Tumorigenesis}, url = {http://dx.doi.org/10.1128/MCB.22.11.3842-3851.2002}, volume = {22}, year = {2002} }

TY - JOUR ID - citeulike:4847394 L3 - citeulike-article-id:4847394 N2 - PTEN is mutated at high frequency in many primary human cancers and several familial cancer predisposition disorders. Activation of AKT is a common event in tumors in which the PTEN gene has been inactivated. We previously showed that deletion of the murine Pten gene in embryonic stem (ES) cells led to increased phosphatidylinositol triphosphate (PIP3) accumulation, enhanced entry into S phase, and better cell survival. Since PIP3 controls multiple signaling molecules, it was not clear to what degree the observed phenotypes were due to deregulated AKT activity. In this study, we mutated Akt-1 in Pten-/- ES cells to directly assess the role of AKT-1 in PTEN-controlled cellular processes, such as cell proliferation, cell survival, and tumorigenesis in nude mice. We showed that AKT-1 is one of the major downstream effectors of PTEN in ES cells and that activation of AKT-1 is required for both the cell survival and cell proliferation phenotypes observed in Pten-/- ES cells. Deletion of Akt-1 partially reverses the aggressive growth of Pten-/- ES cells in vivo, suggesting that AKT-1 plays an essential role in PTEN-controlled tumorigenesis. 10.1128/MCB.22.11.3842-3851.2002 IS - 11 JF - Mol. Cell. Biol. EP - 3851 TI - Essential Role of AKT-1/Protein Kinase B{alpha} in PTEN-Controlled Tumorigenesis VL - 22 SP - 3842 KW - akt KW - apoptosis KW - esc KW - pten AU - Stiles, Bangyan AU - Gilman, Valeriya AU - Khanzenzon, Natalya AU - Lesche, Ralf AU - Li, Annie AU - Qiao, Rong AU - Liu, Xin AU - Wu, Hong PY - 2002/06/01/ UR - http://dx.doi.org/10.1128/MCB.22.11.3842-3851.2002 ER -