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Vitamin E succinate suppresses prostate tumor growth by inducing apoptosis.

Malafa MP, Fokum FD, Andoh J, Neitzel LT, Bandyopadhyay S, Zhan R, Iiizumi M, Furuta E, Horvath E, Watabe K

Division of GI Tumors, Department of Interdisciplinary Oncology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA. malafamp@moffitt.usf.edu

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.

Published 6 March 2006 in Int J Cancer, 118(10): 2441-7.
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Prostate Cancer Research Today Archive:

Volume 1 (2004)
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