The calcimimetic R-568 induces apoptotic cell death in prostate cancer cells

The calcimimetic R-568 induces apoptotic cell death in prostate cancer cells

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Abstract Background Increased serum level of parathyroid hormone (PTH) was found in metastatic prostate cancers.Calcimimetic R-568 was reported to reduce PTH expression, to suppress cell proliferation and to induce apoptosis in parathyroid cells.In this study, we investigated Eye Drops the effect of R-568 on cellular survival of prostate cancer cells.Methods Prostate cancer cell lines LNCaP and PC-3 were used in this study.

Cellular survival was determined with MTT, trypan blue exclusion and fluorescent Live/Death assays.Western blot assay was utilized to assess apoptotic events induced by R-568 treatment.JC-1 staining was used to evaluate mitochondrial membrane potential.Results In cultured prostate cancer LNCaP and PC-3 cells, R-568 treatment significantly reduced cellular survival in a Belts dose- and time-dependent manner.

R-568-induced cell death was an apoptotic event, as evidenced by caspase-3 processing and PARP cleavage, as well as JC-1 color change in mitochondria.Knocking down calcium sensing receptor (CaSR) significantly reduced R-568-induced cytotoxicity.Enforced expression of Bcl-xL gene abolished R-568-induced cell death, while loss of Bcl-xL expression led to increased cell death in R-568-treated LNCaP cells,.Conclusion Taken together, our data demonstrated that calcimimetic R-568 triggers an intrinsic mitochondria-related apoptotic pathway, which is dependent on the CaSR and is modulated by Bcl-xL anti-apoptotic pathway.