الفهرس 
Study of Possible Effects of Bee Venom, Snake Venom and their Fractions on Prostate Cancer Cell Line (PC3)
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Abstract
Prostate cancer is the most frequently diagnosed cancer and the second leading cause of cancer death among men. Chemotherapy and surgery have undesirable side effects. Snake venom (SV), bee venom (BV) and their bioactive components are unique sources for cancer therapy development. The present study evaluated the anticancer potential of SV, BV and their major components (snake venom phospholipase A2 (svPLA2), melittin (MEL) and bee venom phospholipase A2 (bvPLA2)) against human prostate adenocarcinoma (PC3). Cytotoxicity of test venoms and derivatives was conducted using MTT biochemical assay. Genotoxicity and cell cycle profile was performed using real tine PCR for detection of pro-apoptotic and anti-apoptotic genes as well as the biomarker genes for prostate cancer. Cell arrest accumulation was highlighted using flowcytometry. MTT assay showed that treatment with SV and BV and their major components resulted in cellular morphological changes and significant cytotoxic effects in PC3. The cell viability was concentration dependent. Furthermore, our results indicate that the svPLA2 gives much lower cytotoxic effect than the crude SV in PC3 cells in the highest tested concentration of 100 µg/ml. On the other hand, the major components of BV (bvPLA2 and MEL) showed more potent efficacy on PC3 cells than the crude BV. Interestingly, we showed that SV, svPLA2, BV, bvPLA2 and MEL suppressed the mRNA expression of the anti-apoptotic protein Bcl2, while increased the mRNA expression of the pro-apoptotic protein Bax. Moreover, they decreased the overexpressed prostate tumor marker genes; namely Prostate-Specific Antigen (PSA) and Prostate Cancer Antigen 3 (PCA3). The cell cycle analysis showed that SV and svPLA2 arrested the cell cycle at G0/G1 phase, while BV, bvPLA2 and MEL arrested cell cycle at G2/M phase. In conclusion, our work demonstrated that SV, BV and their major components (svPLA2, bvPLA2, MEL) inhibit prostate cancer possibly via triggering cell cycle arrest and apoptosis. Future studies will help estimate the potential of SV, BV and their major components as anticancer agents for the prevention of human prostate cancer.