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J Biol Chem, Vol. 275, Issue 18, 13812-13818, May 5, 2000

Activated 3',5'-Cyclic AMP-dependent Protein Kinase Is Sufficient to Induce Neuroendocrine-like Differentiation of the LNCaP Prostate Tumor Cell Line*

Michael E. CoxDagger §, Paul D. DeebleDagger §, Eric A. Bissonette||, and Sarah J. Parsons§

From the § Department of Microbiology and Cancer Center, University of Virginia School of Medicine, and || Department of Health Evaluation Sciences, University of Virginia Health Systems, Charlottesville, Virginia 22908

Neuroendocrine (NE) differentiation within prostate tumors is proposed to be a contributing factor in disease progression. However, the cellular origin and molecular mechanism controlling differentiation of prostatic NE cells are unresolved. The prostate tumor cell line, LNCaP, can reversibly acquire many NE characteristics in response to treatment with beta -adrenergic receptor agonists and activators of adenylate cyclase. In this study, we demonstrate that these treatments induce protein kinase A (PKA) activation in LNCaP cells and that ectopic expression of a constitutively activated form of the PKA catalytic subunit, CIalpha , results in acquisition of NE characteristics, including the extension of neuritic processes, cessation of mitotic activity, and production of neuron-specific enolase. Forskolin-, epinephrine-, and isoproterenol-dependent NE differentiation of LNCaP cells was significantly inhibited by expressing a dominant negative mutant of the PKA regulatory subunit, RIalpha . These results demonstrate that prostatic NE differentiation in response to these agents depends on PKA activation, and this signaling pathway may provide a therapeutic target for treating advanced forms of prostate cancer.

* This work was supported by National Cancer Institute, National Institutes of Health, Grants PO1 40042, R21 69848, and RO1 76649.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger These authors have contributed equally to this work.

To whom correspondence should be addressed: Dept. of Microbiology, Box 441, University of Virginia Health Sciences Center Charlottesville, VA 22908. Tel.: 804-924-2532; Fax: 804-982-0689; E-mail: mec8 m{at}virginia.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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