Department of Surgery, Veterans Administration San Diego Healthcare System, University of California, 92161, USA.
Cancer Lett. 2011 Jul 1;306(1):52-9. doi: 10.1016/j.canlet.2011.02.027. Epub 2011 Mar 27.
The aim of the study was to demonstrate the role of parathyroid hormone related protein (PTHrP) in stimulating aldo-keto reductase (AKR) 1C3 expression in prostate cancer (CaP) cells. CaP cell proliferation and resistance to apoptosis was increased by PTHrP transfection. Conversely, reducing AKR1C3 expression by siRNA decreased cell proliferation. Since these effects could be mediated through AKR1C3-catalyzed reductions of the PPARγ ligand, 15-DeoxyΔ(12,14)-PGJ(2), we treated the cells with prostaglandins (PG). (PG) D(2) inhibited cell proliferation, but its metabolite, 9α,11β-PGF(2), did not effect CaP cell growth. The AKR1C family members serve as potential therapeutic targets for CaP therapy.
本研究旨在证明甲状旁腺激素相关蛋白（PTHrP）在刺激前列腺癌（CaP）细胞醛酮还原酶（AKR）1C3 表达中的作用。PTHrP 转染可增加 CaP 细胞增殖和抗细胞凋亡能力。相反，通过 siRNA 降低 AKR1C3 表达会降低细胞增殖。由于这些作用可能通过 AKR1C3 催化的 PPARγ 配体 15-脱氧Δ（12,14）-PGJ（2）的还原来介导，我们用前列腺素（PG）处理细胞。（PG）D（2）抑制细胞增殖，但它的代谢物 9α,11β-PGF（2）不会影响 CaP 细胞生长。AKR1C 家族成员可作为 CaP 治疗的潜在治疗靶点。
