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Objective: To investigate the effects of clinically achievable dose of lovastatin on prostate cancer PC3 cells.
Methods: PC3 prostate cancer cells were treated with dimethyl sulfoxide(DMSO),or lovastain only,or lovastatin with mevalonic acid for 24, 48 and 72 hours respectively. MTT assay was used to detect the cell viability. By means of [3H] thymidine incorporation tests, the effects of lovastatin on cell proliferation were analyzed. Western blot was used to detect activated casepase3, caspase7, and cleaved PARP (cPARP), the important molecules on the apoptosis pathway.
Results: Cell proliferation of PC3 was significantly inhibited by 39.29%[(63.69%+/-3.69%) vs (102.98%+/-6.84%), P=0.000] after 48 h treatment with lovastatin at its clinically achievable dose of 2 micromol/L. After 72 hours the cell proliferation was inhibited by 44.24% [(52.79%+/-9.88% ) vs (97.03%+/-0.87%), P=0.048]. The cell number was also markedly decreased (4.86x10(5)+/-0.10x10(5)) vs (9.66x10(5)+/-0.10x10(5)), P=0.000] after 72 h treatment at this low concentration of 2 micromol/L. The viability of PC3 cells was significantly decreased 50.12% (56.52%+/-6.40%) vs (106.64%+/-5.27%), P=0.000] and 60.05% (41.99%+/-11.64%) vs (102.94%+/-8.49%), P=0.000] after 48 h and 72 h treatment, respectively. In addition, 2 micromol/L lovastatin induced activation of casepase7 and led the death substrate PARP to cleavage.
Conclusion: Clinically achievable dose of lovastatin inhibits prostate cancer PC3 cell proliferation and induces PC3 cell apoptosis.
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