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[Cancer Research 60, 3338-3342, July 1, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

Exisulind Induction of Apoptosis Involves Guanosine 3',5'-Cyclic Monophosphate Phosphodiesterase Inhibition, Protein Kinase G Activation, and Attenuated ß-Catenin

W. Joseph Thompson1, Gary A. Piazza, Han Li, Li Liu, John Fetter, Bing Zhu, Gerhard Sperl, Dennis Ahnen and Rifat Pamukcu

Cell Pathways, Inc., Horsham, Pennsylvania 19044 [W. J. T., G. A. P., H. L., L. L., J. F., G. S., R. P.]; Department of Pharmacology, University of South Alabama College of Medicine, Mobile, Alabama 36688 [W. J. T., B. Z.]; and University of Colorado and the Denver Veterans Affairs Medical Center, Denver, Colorado 80220 [D. A.]

Sulindac sulfone (exisulind), although a nonsteroidal anti-inflammatory drug derivative, induces apoptosis in tumor cells by a mechanism that does not involve cyclooxygenase inhibition. SW480 colon tumor cells contain guanosine 3',5'-monophosphate (cGMP) phosphodiesterase (PDE) isoforms of the PDE5 and PDE2 gene families that are inhibited by exisulind and new synthetic analogues. The analogues maintain rank order of potency for PDE inhibition, apoptosis induction, and growth inhibition. A novel mechanism for exisulind to induce apoptosis is studied involving sustained increases in cGMP levels and cGMP-dependent protein kinase (PKG) induction not found with selective PDE5 or most other PDE inhibitors. Accumulated ß-catenin, shown to be a substrate for PKG, is decreased by exisulind, suggesting a mechanism to explain apoptosis induction in neoplastic cells harboring adenomatous polyposis coli gene mutations.




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