Premium
Suppression of prostate cancer in a transgenic rat model via γ‐tocopherol activation of caspase signaling
Author(s) -
Takahashi Satoru,
Takeshita Kentaro,
Seeni Azman,
Sugiura Satoshi,
Tang Mingxi,
Sato Shinya,
Kuriyama Hiroki,
Nakadate Masao,
Abe Koichi,
Maeno Yoshitaka,
Nagao Masataka,
Shirai Tomoyuki
Publication year - 2009
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20915
Subject(s) - prostate cancer , prostate , tocopherol , testosterone (patch) , vitamin e , endocrinology , medicine , cancer , in vivo , tramp , apoptosis , adenocarcinoma , cancer research , biology , biochemistry , antioxidant , microbiology and biotechnology
BACKGROUND Epidemiological data indicate that intake of one form of vitamin E, γ‐tocopherol, may reduce prostate cancer risk, and several in vitro studies have demonstrated that γ‐tocopherol can inhibit prostate cancer cell growth. The purpose of the present study was to confirm effects of γ‐tocopherol on prostate cancer in the transgenic rat for adenocarcinoma of prostate (TRAP) model established in our laboratory. METHODS In Experiment 1, heterozygous male TRAP rats 5 weeks of age received α‐tocopherol at the concentration of 50 mg/kg in the diet, or γ‐tocopherol at 50 or 100 mg/kg for 10 weeks. In Experiment 2, TRAP rats of 3 weeks of age were given γ‐tocopherol at 50, 100, or 200 mg/kg diet for 7 weeks. RESULTS γ‐Tocopherol did not affect body weight gain, organ weights or serum levels of either testosterone or estradiol. However, quantitative evaluation of prostatic lesions demonstrated significantly suppression of sequential progression from PIN to adenocarcinoma in a dose‐dependent manner, along with clear activation of caspases 3 and 7 in the ventral lobe in both experiments. CONCLUSIONS The present study clearly demonstrated that γ‐tocopherol suppresses prostate tumor progression in an in vivo TRAP model, and could be a candidate chemopreventive agent for human prostate cancer. Prostate 69:644–651, 2009. © 2009 Wiley‐Liss, Inc.