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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?5mol/LLaCl3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.
To investigate the potential pharmacological effects of rare earth compounds in the prevention and treatment of prostate cancer metastasis, the effects and mechanisms of lanthanum chloride on the growth and migration of human prostate cancer cell line DU145 were studied.According to MTT results, LaCl3 significantly inhibited the proliferation of DU145 cells , And in a concentration-dependent manner.Clone formation assay also showed that LaCl3 inhibited the formation of clones.The results showed that LaCl3 could inhibit the growth of prostate cancer cells.Furthermore, scratch damage experiments showed that 10-5mol / LLaCl3 could inhibit cell migration and At this concentration, LaCl3 also inhibited the cell adhesion and extension.More studies have shown that different concentrations of LaCl3 can down-regulate the phosphorylation of ERK and P38, and pertussis toxin PTx, a Gi protein inhibitor, weakened LaCl3 On the phosphorylation of ERK and P38 and its inhibition on the formation and expansion of DU145 cells.The results showed that LaCl3 can inhibit the growth and migration of DU145 prostate cancer cells, which may be related to the decrease of phosphorylation of ERK and P38, Is mediated through the PTx-sensitive Gi protein signaling pathway.