Recent years, the incidence and mortality of
prostate cancer have increased dramatically in China. At earlier stages, most diagnosed
prostate cancers are responsive to
androgen depletion treatment, yet, nearly all patients will eventually progress to metastatic
androgen-independent
prostate cancer (
AIPC), which still has no effective therapeutic method or
drug to deal with.
11'-Deoxyverticillin A (C42) belongs to the family of epipolythiodioxopiperazines (ETPs), an interesting class of
fungal toxins that inhibit farnesyl
transferase. Compounds holding such a property have been explored as putative
anticancer agents. In this study, using PC3M cells, an
AIPC cell line, we investigated the effect of the compound on apoptosis and explored the underlying mechanism. It revealed that C42 markedly enhanced the activity of
caspase-3/7 and increased the accumulation of the cleaved PARP, all of which are the markers of apoptosis. It also revealed that C42 either decreased cell viability or inhibited the growth of PC3M cells. Moreover, we observed that the loss of cell viability and cell growth inhibition induced by C42 were both time- and dosage dependent. Taken together, we indicated that C42 can induce caspase-dependent apoptosis in
AIPC cells, and the results presented here will broaden our knowledge about the molecular mechanisms by which C42 exerts its anticancer activity, and future work in this direction may provide valuable information in the development of these compounds into effective
cancer therapeutic strategies against
androgen-independent
prostate cancer.