前列腺癌（Pca)的转移是Pca患者致死的重要原因；上皮间质转化（EMT)参与调控癌细胞的转移。因此，研究Pca细胞的EMT及其机制, 可为防治Pca的转移提供新思路。EMT过程将导致众多粘附分子的表达变化；而Akt1分子参与了细胞间粘附分子的表达调控。我们前期发现：在Pca中，敲除Akt1基因，可诱发EMT，并伴有Wnt和TGF-β信号通路改变。据此，我们提出Akt1可能通过Wnt和TGF-β信号通路，调控Pca细胞的EMT，在其转移中发挥重要作用，但尚需实验加以证实。我们拟在建立包括四环素诱导Akt1基因敲除Pca小鼠等多种Pca转移动物模型和Akt1基因敲除Pca细胞的基础上，利用多种方法探讨Akt1基因对Pca转移的影响；并特异性抑制或过表达Wnt和TGF-β通路的关键分子，检测其对EMT及细胞侵袭力的影响，以对Akt1调控EMT的机制进行探讨。

Prostate cancer (Pca) metastasis is the major cause of death for this disease, so far there is no effective treatment, because the mechanism is not clear. Many studies found epithelial mesenchymal transition (EMT) involved in cancer progression and metastasis, suggesting that study the mechanisms of EMT in cancer cells, has important value for comprehensive treatment strategies. Akt1 is an important endothelial barrier regulator which involved in the regulation of cell adhesion molecules. The cell-cell junction protein expression levels change of cancer cells is an important characteristic of EMT. Therefore, the Akt1 might regulate Pca cell metastasis via EMT. To address this hypothesis, Akt1 knockout Pca cells were generated by Crispr-Cas9 technology and Akt1 gene inducible knockout TRAMP+ mice (rtTA-Akt1-TRAMP+ mice) by crossing rtTA-Akt1 mice with TRAMP+ mice. To study the function of Akt1 gene on Pca metastasis, Pca cells invasion and metastasis ability are evaluated by serials experiment in vivo and in vitro. Wnt and TGF-beta pathway inhibitors are used to explore the possible mechanisms by which Akt1 regulates EMT and the possible mechanism of Akt1 regulation of EMT, so as to provide effective target for prevention and treatment of the disease.