肿瘤细胞在复杂的环境中，通常发生代谢重编程、改变其代谢的流向和流量。大部分研究关注肿瘤细胞的有氧糖酵解过程，但对糖异生（gluconeogenesis）的研究少见。我们近期鉴定了miR301参与调控前列腺癌增殖与糖代谢的新通路，并发现了一些新特点（Cancer Letters, 2018）。最近通过环状RNA芯片筛选，新发现circ87在激素抵抗性前列腺癌（HRPC）组织的表达较正常组织下调，但具体机制未明。生物信息学与预实验结果发现circ87可结合miR301。本项目拟进一步探索circ87通过海绵样吸附抑制miR301、靶向调控糖异生关键酶果糖-1,6-二磷酸酶1(FBP1)，抑制糖异生，导致糖酵解与糖异生失衡、促进前列腺癌细胞增殖的作用机制，并通过动物体内实验与临床前列腺标本染色研究，评价该信号通路对前列腺癌病程进展与预后的预测价值。

To survive in the complicated environment, tumor cells usually choose metabolic reprogramming, to change the metabolic flow volume and flux for fast energy and growth materials supply. Most studies focus on glycolysis, few study has paid attention to gluconeogenesis. Recently,we have identified a new pathway regulated by miR301，which plays an important role in the regulation of proliferation and glucose metabolism (Cancer Letters，2018). We found that circ87 was down-regulated in the hormon-refractory prostate cancer（HRPC）tissues by circular RNA arry analysis. However, the mechanism remains unknown. This programm aims to eluciate the mechanism of circ87 in the regulation of the balance of glycolysis and gluconeogenesis, by sponging with miR301, targeting fructose-1, 6-biphosphate 1 (FBP1 ), suppressing gluconeogenesis pathway.In vivo animal studies and clinical prostatic tissues staining will be used to evaluate the clinical progression and the prognosis value of circ87-miR301-FBP1 signaling in HRPC patients.