Conclusion

With reference to our hypothesis that AR positive stromal cells inhibit the growth of PC3 cells in the presence of androgen, we also analyzed and found similar results while using LNCaP cells. However, the magnitude of growth inhibition was less significant in LNCaP cells as compared to PC3 cells.

Therefore, there is a need to re-identify the role of continued androgen deprivation therapy (ADT) during progression to CRPC. It may be possible that due to androgen deprivation, the growth promoting stromal effects counteract the apoptotic effects of androgen ablation on epithelial cells. On the contrary, the growth inhibiting effects of the stromal AR are lost during ADT. The permanent methods of androgen ablation such as surgical castration can be replaced by reversible methods of castration such as medical castration with LHRH analogues. Interestingly, some investigators have even observed that using androgen replacement therapy (ART) in metastatic CRPC displayed biochemical improvement in patients [24]. Newer therapies targeting the prostate cancer stromal cells should be evaluated.

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