氯化镧抑制前列腺癌细胞DU145 的生长和迁移

为探索稀土化合物在防治前列腺癌转移方面的潜在药理作用, 研究了氯化镧对人前列腺癌细胞DU145 的生长和迁移的影响及其机理. 基于MTT 实验结果得知, LaCl₃ 显著抑制DU145 细胞的增殖, 且呈浓度依赖关系; 克隆形成实验也显示了LaCl₃ 抑制克隆形成. 结果表明, LaCl₃ 能够抑制前列腺癌细胞的生长. 此外, 利用划痕损伤实验证明, 10^?5 mol/L LaCl3 可以抑制细胞迁移, 并且在该浓度下, LaCl₃ 对细胞黏附和伸展也有抑制作用. 进一步的机制研究表明, 不同浓度LaCl₃ 均可下调ERK 和P38 的磷酸化水平; 而百日咳毒素PTx, 一种Gi 蛋白抑制剂, 减弱了LaCl₃ 对ERK 和P38 磷酸化的抑制作用以及其对DU145 细胞克隆形成和伸展的抑制作用. 结果表明, LaCl₃ 能够抑制前列腺癌细胞DU145 的生长和迁移, 该作用与ERK 和P38 磷酸化水平降低有关, 可能是通过PTx 敏感的Gi 蛋白信号通路介导的.

Lanthanum inhibits prostate cancer Du145 cells growth and migration

Lanthanides compounds have been reported to perform anticancer activity in certain cancer cells, but there have been few reports looking specifically at the effects of these compounds on prostate cancer. In this study, we evaluated the effects of lanthanum chloride (LaCl₃) on the proliferation, adhesion and migration ability of androgen-independent prostate cancer DU145 cells. The results of MTT assay showed that LaCl3 treatment inhibited the proliferation of DU-145 cells in a dose-dependent manner. Using colony forming assay, LaCl₃ treatment led to reduced colony forming ability of DU145 cells. Further observations demonstrated that the presence of LaCl₃ decreased adhesive capacity, cell-surface area and migration in DU145 cells. In addition, LaCl₃ treatment inhibited phosphorylation of extracellular signal-regulated kinase (ERK) and P38 MAPK kinase of DU145 cells. Moreover, pretreatment of the cells with pertussis toxin (PTx), a Gi protein inhibitor, abolished LaCl₃-induced ERK and P38 phosphorylation, as well as colony formation and cell-surface area. In conclusion, the findings suggest that LaCl₃ inhibits in vitro DU145 cells growth and migration, and the effect is partly linked to Gi protein signaling pathway.