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Decursin Suppresses Human Androgen-Independent PC3 Prostate Cancer Cell Proliferation by Promoting the Degradation of -Catenin

College of Pharmacy, Chungnam National University, Daejeon, Korea (G.-Y.S., J.-H.L.); PharmcoGenomics Research Center, Inje University, Busan, Korea (M.C., S.O.); Institute of Ecological Phytochemistry, Hankyang National University, Ansung, Korea (B.-S.P.); and Department of Bioscience and Biotechnology, Konkuk University, Seoul, Korea (D.-E.K.)

Alterations in the Wnt/-catenin pathway are associated with the development and progression of human prostate cancer. Decursin, a pyranocoumarin isolated from the Korean Angelica gigas root, inhibits the growth of androgen-independent human prostate cancer cells, but little is known about its mechanism of action. Using a cell-based screen, we found that decursin attenuates the Wnt/-catenin pathway. Decursin antagonized -catenin response transcription (CRT), which was induced with Wnt3a-conditioned medium and LiCl, by promoting the degradation of -catenin. Furthermore, decursin suppressed the expression of cyclin D1 and c-myc, which are downstream target genes of -catenin and thus inhibited the growth of PC3 prostate cancer cells. In contrast, decursinol, in which the (CH₃)₂–C=CH–COO–side chain of decursin is replaced with–OH, had no effect on CRT, the level of intracellular -catenin, or PC3 cell proliferation. Our findings suggest that decursin exerts its anticancer activity in prostate cancer cells via inhibition of the Wnt/-catenin pathway.

Address correspondence to: Dr. Sangtaek Oh, PharmcoGenomics Research Center, Inje University, Busan 614-735, Korea. E-mail: ohsa{at}inje.ac.kr