Vitamin E succinate suppresses prostate tumor growth by inducing apoptosis.

Malafa, Mokenge P.; Fokum, Frida D.; Andoh, Jennifer; Neitzel, Leslie T.; Bandyopadhyay, Sucharita; Zhan, Rui; Iiizumi, Megumi; Furuta, Eiji; Horvath, Elizabeth; Watabe, Kounosuke

Prostate cancer is a major cause of cancer death and morbidity in western countries. However, because of its intrinsic nature of chemoresistance, there is only limited systemic therapy available for the patients. Vitamin E (VE) has been under intensive study as a chemopreventive agent for various types of cancers. Preclinical studies suggest that vitamin E succinate (VES) is the most effective antitumor analogue of VE, yet there are scarce studies of VES in prostate cancer. In this study, we investigated the effects of VES on a panel of prostate cancer cells, and a xenograft model of prostate cancer. Our results indicate that VES significantly inhibited proliferation and induced apoptosis of prostate cancer cell lines in a dose and time dependent manner. The results of microarray analysis followed by real-time RT-PCR and inhibitor analyses indicated that the VES-induced apoptosis is mediated by caspase-4 in prostate tumor cells. In our animal model of prostate cancer in SCID mouse, daily injection of VES significantly suppressed tumor growth as well as lung metastases. These results suggest a potential therapeutic utility of VES for patients with prostate cancer. © 2005 Wiley-Liss, Inc.

International Journal of Cancer, 2006, Vol 118, Issue 10, p2441

0020-7136

Academic Journal

10.1002/ijc.21689