Molecular Effects of 13C/DIM in Prostate Cancer
Annual rept. 1 Apr 2003-31 Mar 2004
WAYNE STATE UNIV DETROIT MI
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Our previous data have shown that I3C inhibits cell growth and induces apoptosis in cancer cells. We have also observed a reduction in the activated Akt and the activity of NF-xB in prostate cancer cells treated with I3C We hypothesize that I3CDIM functions as an inhibitor of NF-xB, which may be due to the inactivation of Akt-related signaling molecules, and ultimately leads to the induction-of-apoptotic processes. To test our hypotheses we investigated the effects of I3CDIM on NF-xB and Akt activities in prostate cancer-cells and non-tumorigenic prostate epithelial cells. We also investigated how the Akt and NF-cB pathways may cross-talk in prostate cancer cells exposed to I3CDIM. We have found that 13CDIM inhibited NF-xB activity and the inhibition- was partly mediated through the inactivation of Akt. 13C and DIM inactivated NF-KB and Akt, f regulated the expressi9n of genes related to cell growth and apoptosis, and induced Bax trans location and cytochrome c release, resulting in inhibition of cell growth and induction of apoptosis in prostate cancer cells. However, no significant such effects were observed in non-tumorigenic CRt-222l prostate epithelial cells, suggesting that I3C and DIM may be potent agents for the prevention andor treatment of prostate cancer.
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