摘要
目的:研究丹参酮对雄激素剥夺治疗(ADT)促发的前列腺癌细胞侵袭的影响,并探讨可能机制。方法:人前列腺癌LNCaP细胞分为对照组、丹参酮1组、丹参酮2组、丹参酮3组,分别采用0、5、10、20 nmol/L丹参酮处理。平板克隆实验检测克隆能力,管腔形成实验检测血管生成能力,Transwell小室实验检测侵袭能力,AnnexinV-FITC/PI双染法检测细胞凋亡率,Western印迹法检测细胞磷脂酰肌醇3激酶(PI3K)、p-PI3K、蛋白激酶B(AKT)、p-AKT蛋白表达量。结果:对照组、丹参酮1组、丹参酮2组、丹参酮3组细胞克隆形成率、管腔数量、穿膜细胞数量、细胞凋亡率、p-PI3K/PI3K、p-AKT/AKT比较,差异有统计学意义(P<0.05);与对照组比较,丹参酮1组细胞克隆形成率更低(P<0.05),管腔数量更少(P<0.05),穿膜细胞数量更少(P<0.05),细胞凋亡率更高(P<0.05),p-PI3K/PI3K、p-AKT/AKT更低(P<0.05);与丹参酮1组比较,丹参酮2组细胞克隆形成率更低(P<0.05),管腔数量更少(P<0.05),穿膜细胞数量更少(P<0.05),细胞凋亡率更高(P<0.05),p-PI3K/PI3K、p-AKT/AKT更低(P<0.05);与丹参酮2组比较,丹参酮3组细胞克隆形成率更低(P<0.05),管腔数量更少(P<0.05),穿膜细胞数量更少(P<0.05),细胞凋亡率更高(P<0.05),p-PI3K/PI3K、p-AKT/AKT更低(P<0.05)。结论:丹参酮可逆转ADT促发的前列腺癌细胞侵袭,并降低细胞克隆、血管形成能力,促进细胞凋亡,抑制PI3K/AKT信号通路活性。
Objective:To explore the effect of tanshinone on the invasion of PCa cells induced by androgen-deprivation therapy(ADT)and its possible action mechanism.Methods: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.Results: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).Conclusion: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.
作者
马漫遥
徐文
MA Man-yao;XU Wen(School of Pharmacy,Shandong University of Chinese Medicine,Jinan,Shandong 250355,China)
出处
《中华男科学杂志》
CAS
CSCD
2024年第2期104-110,共7页
National Journal of Andrology
基金
山东省高等教育本科教学改革研究项目(M2022137)
山东省中医药健康养老服务现状分析及对策研究(2019-0006)
关键词
雄激素剥夺治疗
前列腺癌
丹参酮
侵袭
androgen-deprivation therapy
prostate cancer
tanshinone
invasion
