目的探讨丹参酮对雄激素剥夺疗法（ADT）诱导的PCa细胞侵袭的影响及其可能的作用机制。我们分别用0 nmol/L（对照组）、5 nmol/L丹参酮处理人PCa LNCaP细胞。分别为（丹参酮组 1）、10 nmol/L（丹参酮组 2）和 20 nmol/L（丹参酮组 3）。分别采用平板克隆实验、管形成实验和Transwell小室实验检测其克隆、血管生成和侵袭能力，采用AnnexinV-FITC/PI双染法检测其凋亡情况，并测定磷脂酰肌醇3-激酶的蛋白表达。 Western blot检测PI3K、p-PI3K、蛋白激酶B(AKT)和p-AKT。与对照组相比，丹参酮1、2、3组的PCa LNCaP细胞克隆出现明显的剂量依赖性下降。形成率（［25.14±5.19］% vs ［19.33±4.12］% vs ［14.69±4.71］% vs ［9.35±2.37］%，P<0.05）、细胞腔数（［23.20±4.85］ vs ［19.80±）每个显微视野中的5.12] vs [14.40 ± 4.16] vs [10.20 ± 3.21]，P<0.05）和跨膜细胞计数（[62.80 ± 8.97] vs [50.40 ± 7.62] vs [38.60 ± 5.16] vs [27.40 ± 4.91] ］每视野，P<0.05），细胞凋亡率增加（［3.58±0.74］% vs ［8.97±1.36］% vs ［14.64±4.10］% vs ［21.17±5.37］%，P<0.05） ，下调 p-PI3K、PI3K、p-AKT 和 AKT 的表达（P<0.05）。丹参酮可以逆转 ADT 诱导的 PCa 细胞侵袭，减少其克隆形成和血管生成，促进其凋亡，并抑制PI3K 和 AKT 信号通路的活性。

To explore the effect of tanshinone on the invasion of PCa cells induced by androgen-deprivation therapy (ADT) and its possible action mechanism.We treated human PCa LNCaP cells with tanshinone at 0 nmol/L (the control group), 5 nmol/L (tanshinone group 1), 10 nmol/L (tanshinone group 2) and 20 nmol/L (tanshinone group 3), respectively. Then we detected their cloning, angiogenesis and invasion abilities by plate cloning assay, tube-formation assay and Transwell chamber assay, respectively, examined their apoptosis using the AnnexinV-FITC/PI double staining method, and determined the protein expressions of phosphatidylinositol 3-kinase (PI3K), p-PI3K, protein kinase B (AKT) and p-AKT by Western blot.Compared with the control group, the PCa LNCaP cells in the tanshinone groups 1, 2 and 3 showed significant dose-dependent decreases in the clone formation rate (［25.14 ± 5.19］% vs ［19.33 ± 4.12］% vs ［14.69 ± 4.71］% vs ［9.35 ± 2.37］%, P<0.05), number of cellular lumens (［23.20 ± 4.85］ vs ［19.80 ± 5.12］ vs ［14.40 ± 4.16］ vs ［10.20 ± 3.21］ per microscopic field, P<0.05) and count of transmembrane cells (［62.80 ± 8.97］ vs ［50.40 ± 7.62］ vs ［38.60 ± 5.16］ vs ［27.40 ± 4.91］ per microscopic field, P<0.05), increase in the rate of cell apoptosis (［3.58 ± 0.74］% vs ［8.97 ± 1.36］% vs ［14.64 ± 4.10］% vs ［21.17 ± 5.37］%, P<0.05), and down-regulation of the expressions of p-PI3K, PI3K, p-AKT and AKT (P<0.05).Tanshinone can reverse ADT-induced invasion of PCa cells, reduce their clone formation and angiogenesis, promote their apoptosis, and inhibit the activity of PI3K and AKT signaling pathways.