Abstract
IntroductionApoptosis is down regulated in most forms of cancer. Mitochondria are central to the apoptotic process and are targeted in cancer therapy by novel drug candidates. Calliandra portoricensis (CP) is used in the management of prostate enlargement in folk medicine. This study was designed to investigate the effects of CP on mitochondrial-mediated apoptosis and cell proliferation using prostate cancer cells.Material and methodsProstate cancer cells were treated with methanol fraction of CP (MFCP), cell cycle analysis was evaluated by flow cytometry and levels of pro-apoptotic Bax, anti-apoptotic Bcl-2, Cytochrome C Release and activation of caspases 3and 9 were determined using ELISA kits.Results and discussionsThe MFCP inhibited (p<0.05) proliferation of prostatic cancer cells. The growth inhibition by MFCP (10 µg/mL) correlated with a 3-fold decreased expression of Bcl-2 and a 4-fold increase in Bax levels in LNCaP cells. The MFCP (10 µg/mL) activated C3 and C9 at by 4.2 and 5.1 folds over control, respectively which prompted cancer cells to arrest at S phase. The LC-MS analysis revealed the presence of polyphenols in MFCP.ConclusionTaken together, MFCP- induced cell death is mediated by alteration of mitochondrial integrity and cell cycle arrest. Hence, MFCP may be effective for cancer pharmacotherapy.
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