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[Cancer Research 60, 1541-1545, March 15, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

Modulation of Hypoxia-inducible Factor 1{alpha} Expression by the Epidermal Growth Factor/Phosphatidylinositol 3-Kinase/PTEN/AKT/FRAP Pathway in Human Prostate Cancer Cells: Implications for Tumor Angiogenesis and Therapeutics1

Hua Zhong, Kelly Chiles, David Feldser, Erik Laughner, Colleen Hanrahan, Maria-Magdalena Georgescu, Jonathan W. Simons2 and Gregg L. Semenza

The Johns Hopkins Oncology Center, Brady Urological Institute [H. Z., C. H., J. W. S.] and Departments of Pediatrics and Medicine and Institute of Genetic Medicine [K. C., D. F., E. L., G. L. S.], The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, and Laboratory of Molecular Oncology, The Rockefeller University, New York, New York 10021 [M-M. G.]

Dysregulated signal transduction from receptor tyrosine kinases to phosphatidylinositol 3-kinase (PI3K), AKT (protein kinase B), and its effector FKBP-rapamycin-associated protein (FRAP) occurs via autocrine stimulation or inactivation of the tumor suppressor PTEN in many cancers. Here we demonstrate that in human prostate cancer cells, basal-, growth factor-, and mitogen-induced expression of hypoxia-inducible factor 1 (HIF-1) {alpha}, the regulated subunit of the transcription factor HIF-1, is blocked by LY294002 and rapamycin, inhibitors of PI3K and FRAP, respectively. HIF-1-dependent gene transcription is blocked by dominant-negative AKT or PI3K and by wild-type PTEN, whereas transcription is stimulated by constitutively active AKT or dominant-negative PTEN. LY294002 and rapamycin also inhibit growth factor- and mitogen-induced secretion of vascular endothelial growth factor, the product of a known HIF-1 target gene, thus linking the PI3K/PTEN/AKT/FRAP pathway, HIF-1, and tumor angiogenesis. These data indicate that pharmacological agents that target PI3K, AKT, or FRAP in tumor cells inhibit HIF-1{alpha} expression and that such inhibition may contribute to therapeutic efficacy.




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