Abstract
Emergence of an untreatable hormone refractory status, HRPC, is an inevitable outcome for most patients diagnosed with prostate cancer. Our long-term research interest is to develop prevention and treatment strategies for HRPC. In this study, we tested whether a novel purine, reversine, reportedly capable of inducing cell de-differentiation, might promote the phenotypic re-establishment of HRPC in the form of clinically treatable, androgen-responsive state. We found that sub-μM reversine suppressed clonogenicity, inhibited proliferation, induced G2/M arrest, and enhanced apoptosis in PC-3 cells, an in vitro model of HRPC. We also observed that reversine was significantly less growth inhibitory in normal prostate stromal cell. Further analysis of cell cycle regulatory protein expression in control and reversine-treated PC-3 cell showed that reversine controls G2/M traverse and induces apoptosis in HRPC by regulating the functions, location and turnover of cdc25c, a pivotal G2/M checkpoint sensor. The results suggest that reversine is preferentially active in HRPC.
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