Laboratory analyses of PC-SPES indicate the presence of estrogenic compounds different from diethylstilbestrol, estrone, and estradiol. In vitro testing of this extract shows suppressed cell proliferation and reduced clonogenicity in human tumor cell lines, including prostate, breast, and colon cancers. The predominant cell cycle effect induced by PC-SPES is prolongation of G1 phase. However, apoptosis was observed after exposure of tumor cells to PC-SPES for 48 hours or longer. PC-SPES also inhibits proliferation of LNCaP prostate cell lines, and was associated with a 60–70% downregulation of the proliferating cell nuclear antigen. Preliminary studies evaluating the viability of prostate cancer cell lines LNCaP, LNCaP apoptosis-resistant derivative, LNCaP-bcl-2, PC3, and DU145 at three concentrations of PC-SPES show inhibited growth at concentrations of 4 mcg/mL or less. Another in vitro study indicates its cytotoxicity may be due to alteration of specific gene expressions involved in regulating the cell cycle, cell structure, and androgen response. No single botanical or chemical extract appears responsible for the overall effects of this product. PC-SPES batches used in clinical studies have been found to contain small amounts of diethylstibestrol and ethinyl estradiol, but it is unclear whether these agents account for its anticancer effects.
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