SEATTLE – May 31, 2002 -- Scientists have discovered for the first time how vitamin E interferes with internal cell mechanisms to prevent or slow the growth of prostate cancer.

The discovery opens up new lines of research that may improve on current treatments aimed at blocking the protein receptors prostate cancer cells use to fuel growth and spread or metastasize to other parts of the body.

Earlier large population studies had shown that vitamin E could reduce the development of prostate cancer, but scientists remained puzzled by the underlying biological mechanism that could account for the finding.

The research team led by Dr. Shuyuan Yeh of the University of Rochester, Rochester, NY reported in the May 28, 2002 Proceedings of the National Academy of Science, that the common vitamin works by suppressing production of two key proteins associated with prostate cancer growth, the prostate specific antigen (PSA) and the androgen receptor.

“Our data indicate that VES (vitamin E) may suppress androgen/androgen receptor-mediated cell growth and PSA expression by inhibiting AR expression (production),” the researchers wrote. “This previously undescribed mechanism may explain how VES inhibits the growth of prostate cancer cells and help us to establish new therapeutic concepts for the prevention and treatment of prostate cancer.”

In the laboratory experiments, the researchers studied the effects of vitamin E on the internal mechanisms within prostate cancer cells that depend on androgens or hormones, including testosterone, to grow. They also compared the effect of vitamin E on prostate cancer cells that were also treated with a commonly prescribed hormone suppression drug called hydroxyflutamide (HF).

Specifically, they found that vitamin E interfered with prostate cancer cells’ ability to manufacture androgen receptors, which prostate cancer cells need to make use of testosterone to stimulate cell growth.

With the suppression of androgen receptors, the scientists found that production of PSA did not rise to the levels it usually does in prostate cancer cells, suggesting that PSA levels are dependent on androgen receptor production.

The researchers theorize that this dual action of vitamin E may have the further effect of keeping other genes associated with prostate cancer from becoming active.

In an additional experiment, the researchers did not publish, they found that the antioxidant effect of vitamin E probably cannot explain its ability to suppress the production of androgen receptor. They tried the same experiment using ascorbic acid (vitamin C), which has a stronger antioxidant effect than the type of vitamin E they had used and found that vitamin C did little to suppress AR production.

In comparing the effects of vitamin E to the anti-androgen drug HF, they found that vitamin E was more effective in suppressing the growth of the prostate cancer cells than HF, but that the combination of vitamin E and HF was more effective in slowing or stopping the cancer cell growth than either compound alone.

“This combination (of vitamin E and HF) may have potential for clinical treatment and should warrant further study,” the researchers concluded.

SOURCE: Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 11, 7408-7413,

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