In recent years, several studies have shown that
vitamin k2 (VK2) has anticancer activity in a variety of
cancer cells. The antitumor effects of VK2 in
prostate cancer are currently not known. In the present study, we sought to characterize the anticancer potential of VK2 in both
androgen-dependent and -independent
prostate cancer cells. Our investigations show that VK2 is able to suppress viability of
androgen-dependent and
androgen-independent
prostate cancer cells via
caspase-3 and -8 dependent apoptosis. We also show that VK2 treatment reduces
androgen receptor expression and PSA secretion in
androgen-dependent
prostate cancer cells. Our results also implicate VK2 as a potential
anti-inflammatory agent, as several inflammatory genes are downregulated in
prostate cancer cells following treatment with VK2. Additionally, AKT and
NF-kB levels in
prostate cancer cells are reduced significantly when treated with VK2. These findings correlated with the results of the Boyden chamber and angiogenesis assay, as VK2 treatment reduced cell migration and angiogenesis potential of
prostate cancer cells. Finally, in a nude mice model, VK2 administration resulted in significant inhibition of both
androgen-dependent and
androgen-independent
tumor growth. Overall, our results suggest that VK2 may be a potential therapeutic agent in the treatment of
prostate cancer.