Multiple Signaling Pathways of the Insulin-Like Growth Factor 1 Receptor in Protection from Apoptosis

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Molecular and Cellular Biology, October 1999, p. 7203-7215, Vol. 19, No. 10
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Multiple Signaling Pathways of the Insulin-Like Growth Factor 1 Receptor in Protection from Apoptosis

Francesca Peruzzi, Marco Prisco, Michael Dews, Paolo Salomoni, Emanuela Grassilli, Gaetano Romano, Bruno Calabretta, and Renato Baserga^*

Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107

Received 3 March 1999/Returned for modification 27 April 1999/Accepted 15 July 1999

The type 1 insulin-like growth factor receptor (IGF-1R), activated by its ligands, protects several cell types from a varietyof apoptotic injuries. The main signaling pathway for IGF-1R-mediatedprotection from apoptosis has been previously elucidated and restson the activation of phosphatidylinositol 3-kinase, Akt/proteinkinase B, and the phosphorylation and inactivation of BAD, a memberof the Bcl-2 family of proteins. In 32D cells (a murine hemopoieticcell line devoid of insulin receptor substrate 1 [IRS-1]), theIGF-1R activates alternative pathways for protection from apoptosisinduced by withdrawal of interleukin-3. One of these pathwaysleads to the activation of mitogen-activated protein kinase, whilea third pathway results in the mitochondrial translocation ofRaf and depends on the integrity of a group of serines in theC terminus of the receptor that are known to interact with 14.3.3proteins. All three pathways, however, result in BAD phosphorylation.The presence of multiple antiapoptotic pathways may explain theremarkable efficacy of the IGF-1R in protecting cells fromapoptosis.

^* Corresponding author. Mailing address: Kimmel Cancer Center, Thomas Jefferson University, 624 Bluemle Life Sciences Building,233 S. 10th St., Philadelphia, PA 19107. Phone: (215) 503-4507.Fax: (215) 923-0249. E-mail: r_baserga{at}lac.jci.tju.edu.

Molecular and Cellular Biology, October 1999, p. 7203-7215, Vol. 19, No. 10
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

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Krause, D., Lyons, A., Fennelly, C., O'Connor, R. (2001). Transient Activation of Jun N-terminal Kinases and Protection from Apoptosis by the Insulin-like Growth Factor I Receptor Can Be Suppressed by Dicumarol. J. Biol. Chem. 276: 19244-19252 [Abstract] [Full Text]
Belletti, B., Prisco, M., Morrione, A., Valentinis, B., Navarro, M., Baserga, R. (2001). Regulation of Id2 Gene Expression by the Insulin-like Growth Factor I Receptor Requires Signaling by Phosphatidylinositol 3-Kinase. J. Biol. Chem. 276: 13867-13874 [Abstract] [Full Text]
Khatib, A.-M., Siegfried, G., Prat, A., Luis, J., Chretien, M., Metrakos, P., Seidah, N. G. (2001). Inhibition of Proprotein Convertases Is Associated with Loss of Growth and Tumorigenicity of HT-29 Human Colon Carcinoma Cells. IMPORTANCE OF INSULIN-LIKE GROWTH FACTOR-1 (IGF-1) RECEPTOR PROCESSING IN IGF-1-MEDIATED FUNCTIONS. J. Biol. Chem. 276: 30686-30693 [Abstract] [Full Text]
Peruzzi, F., Prisco, M., Morrione, A., Valentinis, B., Baserga, R. (2001). Anti-apoptotic Signaling of the Insulin-like Growth Factor-I Receptor through Mitochondrial Translocation of c-Raf and Nedd4. J. Biol. Chem. 276: 25990-25996 [Abstract] [Full Text]
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Peretz, S., Jensen, R., Baserga, R., Glazer, P. M. (2001). ATM-dependent expression of the insulin-like growth factor-I receptor in a pathway regulating radiation response. Proc. Natl. Acad. Sci. USA 98: 1676-1681 [Abstract] [Full Text]
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Playford, M. P., Bicknell, D., Bodmer, W. F., Macaulay, V. M. (2000). Insulin-like growth factor 1 regulates the location, stability, and transcriptional activity of beta -catenin. Proc. Natl. Acad. Sci. USA 97: 12103-12108 [Abstract] [Full Text]

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