CG&D
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by van Golen, C. M.
Right arrow Articles by Feldman, E. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by van Golen, C. M.
Right arrow Articles by Feldman, E. L.
Cell Growth & Differentiation Vol. 12, 371-378, July 2001
© 2001 American Association for Cancer Research

PTEN/MMAC1 Overexpression Decreases Insulin-like Growth Factor-I-mediated Protection from Apoptosis in Neuroblastoma Cells1

Cynthia M. van Golen, Tracy S. Schwab, Kathleen M. Woods Ignatoski, Stephen P. Ethier and Eva L. Feldman2

University of Michigan Department of Neurology, Neuroscience Program [C. M. v. G., T. S. S., E. L. F.], and Department of Radiation Oncology [K. M. W. I., S. P. E.], Ann Arbor, Michigan 48109

Insulin-like growth factor I (IGF-I) protects cells from apoptosis primarily through the action of phosphatidylinositol-3 kinase and the downstream serine/threonine kinase Akt. The PTEN gene product, a protein which dephosphorylates phosphatidylinositol lipids, prevents activation of Akt and regulates several cellular functions, including cell cycle progression, cell migration, and survival from apoptosis. In this study, PTEN overexpression decreases IGF-I-induced Akt activity, enhances serum withdrawal-induced apoptosis, and decreases IGF-I protection and cell growth in SHEP cells. The PTEN lipid phosphatase mutant G129E fails to inhibit IGF-I-stimulated Akt activity and protection from apoptosis. The C124S mutation, which abolishes both lipid and protein phosphatase activity, fails to inhibit Akt activity and IGF-I protection against hyperosmotic-induced apoptosis but still inhibits growth and IGF-I protection against serum withdrawal-induced apoptosis. These data suggest a role for PTEN in modulating the effect of IGF-I on Akt activity, neuroblastoma cell growth, and protection against apoptotic stimuli.




This article has been cited by other articles:


Home page
Cancer Res.Home page
D. Opel, C. Poremba, T. Simon, K.-M. Debatin, and S. Fulda
Activation of Akt Predicts Poor Outcome in Neuroblastoma
Cancer Res., January 15, 2007; 67(2): 735 - 745.
[Abstract] [Full Text] [PDF]


Home page
J. Cell Sci.Home page
G. Otaegi, M. J. Yusta-Boyo, E. Vergano-Vera, H. R. Mendez-Gomez, A. C. Carrera, J. L. Abad, M. Gonzalez, E. J. de la Rosa, C. Vicario-Abejon, and F. de Pablo
Modulation of the PI 3-kinase-Akt signalling pathway by IGF-I and PTEN regulates the differentiation of neural stem/precursor cells
J. Cell Sci., July 1, 2006; 119(13): 2739 - 2748.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
J.-L. Liu, X. Sheng, Z. K. Hortobagyi, Z. Mao, G. E. Gallick, and W. K. A. Yung
Nuclear PTEN-Mediated Growth Suppression Is Independent of Akt Down-Regulation
Mol. Cell. Biol., July 15, 2005; 25(14): 6211 - 6224.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
J. T. Lee Jr., L. S. Steelman, and J. A. McCubrey
Phosphatidylinositol 3'-Kinase Activation Leads to Multidrug Resistance Protein-1 Expression and Subsequent Chemoresistance in Advanced Prostate Cancer Cells
Cancer Res., November 15, 2004; 64(22): 8397 - 8404.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
S. Musatov, J. Roberts, A. I. Brooks, J. Pena, S. Betchen, D. W. Pfaff, and M. G. Kaplitt
Inhibition of neuronal phenotype by PTEN in PC12 cells
PNAS, March 9, 2004; 101(10): 3627 - 3631.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
J. H. Lee, K. Y. Kim, Y.-K. Lee, S. Y. Park, C. D. Kim, W. S. Lee, B. Y. Rhim, and K. W. Hong
Cilostazol Prevents Focal Cerebral Ischemic Injury by Enhancing Casein Kinase 2 Phosphorylation and Suppression of Phosphatase and Tensin Homolog Deleted from Chromosome 10 Phosphorylation in Rats
J. Pharmacol. Exp. Ther., March 1, 2004; 308(3): 896 - 903.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
K. W. Hong, K. Y. Kim, H. K. Shin, J. H. Lee, J. M. Choi, Y.-G. Kwak, C. D. Kim, W. S. Lee, and B. Y. Rhim
Cilostazol Prevents Tumor Necrosis Factor-{alpha}-Induced Cell Death by Suppression of Phosphatase and Tensin Homolog Deleted from Chromosome 10 Phosphorylation and Activation of Akt/Cyclic AMP Response Element-Binding Protein Phosphorylation
J. Pharmacol. Exp. Ther., September 1, 2003; 306(3): 1182 - 1190.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
B. Kim and E. L. Feldman
Insulin-like Growth Factor I Prevents Mannitol-induced Degradation of Focal Adhesion Kinase and Akt
J. Biol. Chem., July 26, 2002; 277(30): 27393 - 27400.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 2001 by the American Association of Cancer Research.