Novel indole-3-carbinol-derived antitumor agents

MEDI 337

Jing-Ru Weng, jrweng@mail.cmu.edu.tw1, Chen-Hsun Tsai2, Samuel K. Kulp2, Dasheng Wang2, Chia-Hui Lin2, Yihui Ma2, and Ching-Shih Chen2. (1) Department of Biological Science and Technology, China Medical University, 91 Hsueh-Shih Road, Taichung, 40402, NA, Taiwan, (2) Division of Medicinal Chemistry, College of Pharmacy, The Ohio State University, R. m. 336, 12th Ave., Columbus, OH 43210
Purpose. The chemopreventive potential of indole-3-carbinol has attracted much attention because of its demonstrated ability to protect against chemical-induced carcinogenesis in different experimental animal models. From a mechanistic perspective, the ability of indole-3-carbinol to target a broad range of signaling pathways underlies its translational potential for cancer prevention and/or treatment. Therefore, this study was aimed at pharmacologically exploiting indole-3-carbinol as a molecular platform to develop structural variants with improved chemical stability and apoptosis-inducing potency. Methods. Structural optimization was carried out by structure-activity correlations in conjunction with molecular modeling. The in vitro effects of structural variants vis-à-vis indole-3-carbinol were evaluated in PC-3 and LNCaP human prostate cancer cell lines. Cell viability, apoptosis, and signaling targets were determined by immunoblotting, and chemical stability was assessed by nuclear magnetic resonance spectrometry. Results. Among a series of indole-3-carbinol derivatives examined, OSUMC-A9 represented the optimal agent with IC50 of 2 µM and 3.8 µM for reducing the viability of PC-3 and LNCaP cells, respectively, which were two-order-of-magnitude lower than that of indole-3-carbinol (respective IC50, 512 µM and 267 µM). Despite a 100-fold difference in antitumor potency, the pharmacological profiles of OSUMC-A9 and indole-3-carbinol in interfering with target signaling pathways were virtually identical. Both agents facilitated dose-dependent dephosphorylation of Akt and its substrates GSK3 and Bad, accompanied by increased phosphorylation of MAP kinases. Moreover, the effects of OSUMC-A9 on suppressing the expression of Bcl-2, Bcl-xL, Mcl-1, survivin, NF-kB, and cyclin D1, and on up-regulating the expression of Bax, p27, and p21 paralleled those of indole-3-carbinol. The growth of existing PC-3 tumor xenografts was completely suppressed after i.p. treatment with OSUMC-A9 at 25 mg/kg. Conclusion. OSUMC-A9 is a potent antitumor agent with pleotropic mode of mechanisms by affecting multiple signaling pathways, which might have translational potential in cancer therapy.
 

Poster Session
7:00 PM-9:00 PM, Wednesday, August 22, 2007 BCEC -- Exhibit Hall - B2, Poster

Division of Medicinal Chemistry

The 234th ACS National Meeting, Boston, MA, August 19-23, 2007