Pamidronate inhibits antiapoptotic bcl-2 expression through inhibition of the mevalonate pathway in prostate cancer PC-3 cells.

Bisphosphonates are expected to be efficacious to prevent the growth of metastatic cancer in bone tissue. Bone metastases often occur in patients with various cancers, such as breast, lung and prostate cancer. Bcl-2 is a potent antiapoptotic protein and its expression is known to be closely related to its function.

Protein kinase C is inhibited by bisphosphonates in prostate cancer PC-3 cells.

Bisphosphonates are expected to be effective at preventing tumor metastasis to bone tissue. Since protein kinase C (PKC) plays a crucial role in cancer progression, we examined the effect of bisphosphonates on PKC expression to clarify the mechanism behind the inhibition of the bone metastasis of prostate cancer by bisphosphonates. We found that pamidronate inhibits PKC protein expression and PKC activity in prostate cancer PC-3 cells.

Pamidronate down-regulates urokinase-type plasminogen activator expression in PC-3 prostate cancer cells.

Background: Bisphosphonates are considered to be effective in preventing tumor metastasis to bone. Urokinase-type plasminogen activator (uPA) is thought to be critically involved in the metastatic phenotype of prostate cancer. In this study, we examined the effect of pamidronate on uPA expression in PC-3 prostate cancer cells.