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Molecular and Cellular Biology, January 2000, p. 139-148, Vol. 20, No. 1
0270-7306/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

The Phosphoinositide 3-OH Kinase/AKT2 Pathway as a Critical Target for Farnesyltransferase Inhibitor-Induced Apoptosis

Kun Jiang,1 Domenico Coppola,1 Nichole C. Crespo,2 Santo V. Nicosia,1 Andrew D. Hamilton,3 Said M. Sebti,2,* and Jin Q. Cheng1,*

Department of Pathology1 and Drug Discovery Program and Department of Biochemistry and Molecular Biology,2 College of Medicine and H. Lee Moffitt Cancer Center, University of South Florida, Tampa, Florida 33612, and Department of Chemistry, Yale University, New Haven, Connecticut 065113

Received 21 June 1999/Returned for modification 22 August 1999/Accepted 20 September 1999

Farnesyltransferase inhibitors (FTIs) represent a novel class of anticancer drugs that exhibit a remarkable ability to inhibit malignant transformation without toxicity to normal cells. However, the mechanism by which FTIs inhibit tumor growth is not well understood. Here, we demonstrate that FTI-277 inhibits phosphatidylinositol 3-OH kinase (PI 3-kinase)/AKT2-mediated growth factor- and adhesion-dependent survival pathways and induces apoptosis in human cancer cells that overexpress AKT2. Furthermore, overexpression of AKT2, but not oncogenic H-Ras, sensitizes NIH 3T3 cells to FTI-277, and a high serum level prevents FTI-277-induced apoptosis in H-Ras- but not AKT2-transformed NIH 3T3 cells. A constitutively active form of AKT2 rescues human cancer cells from FTI-277-induced apoptosis. FTI-277 inhibits insulin-like growth factor 1-induced PI 3-kinase and AKT2 activation and subsequent phosphorylation of the proapoptotic protein BAD. Integrin-dependent activation of AKT2 is also blocked by FTI-277. Thus, a mechanism for FTI inhibition of human tumor growth is by inducing apoptosis through inhibition of PI 3-kinase/AKT2-mediated cell survival and adhesion pathway.

* Corresponding author. Mailing address for Jin Q. Cheng: Department of Pathology, College of Medicine/H. Lee Moffitt Cancer Center, University of South Florida, 12901 Bruce B. Downs Blvd., MDC 11, Tampa, FL 33612. Phone: (813) 974-8595. Fax: (813) 974-5536. E-mail: jcheng{at}com1.med.usf.edu. Mailing address for Said M. Sebti: Drug Discovery Program, H. Lee Moffitt Cancer Center, 12902 Magnolia Dr., Tampa, FL 33612. Phone: (813) 979-6734. Fax: (813) 979-6748. E-mail: Sebti{at}moffitt.usf.edu.

Molecular and Cellular Biology, January 2000, p. 139-148, Vol. 20, No. 1
0270-7306/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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