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The Study of Androgen Effects on LPA‐induced ROS in Different Human Prostate Cancer Cell Lines

Treatment of prostate cancer by using androgen deprivation therapy often ensued relapse such as independency of androgen stimulation, producing androgen‐refractory tumors with increased invasion, proliferation, and malignancy. The detailed molecular mechanism of this gradual transition is not clearly understood. Recent reports found that androgen negatively regulates vascular endothelial growth factor‐C (VEGF‐C) effects in prostate cancer cell line. Additionally, androgen deprivation leads to intracellular reactive oxygen species (ROS) generation in rat prostate and also in human prostate cancer cell line LNCaP. Furthermore, our previous study indicated that lysophosphatidic acid (LPA) induces the expression of VEGF‐C through ROS generation in PC‐3 cell, a human androgen‐independent prostate cancer cell line. Therefore, we attempt to investigate whether LPA‐induced ROS generation is affected by androgen in different prostate cancer cells. The flow cytometric analysis results revealed that LPA triggers ROS generation in different prostate cancer cell lines. In addition, our results further demonstrated that androgen agonist Mibolerone decreased LPA‐induced ROS generation. In contrast, LPA‐induced ROS production was enhanced by treatment with androgen antagonist Bicalutamide. In summary, our results demonstrated that androgen might regulate LPA‐induced ROS generation in human prostate cancer cells.