Bikunin抑制前列腺癌细胞PC3体外侵袭的实验研究

目的:探讨bi kuni n对前列腺癌细胞侵袭能力的影响及其相关的分子机制。方法:利用bi kuni n处理前列腺癌细胞系PC3,采用t r ans wel l实验检测其对细胞侵袭能力的影响。同时,利用west ern印迹技术检测PI3K/AKT信号通路在此过程中的作用。结果:Bi kuni n能够显著降低PC3细胞的侵袭能力;Bi kuni n能够抑制PI3K和AKT的活性;PI3K和AKT的抑制剂能够抑制PC3细胞的侵袭;组成型活化的PI3K能够阻断bi kuni n的抑制作用。结论:Bi kuni n可能通过调节PI3K/AKT信号通路来抑制前列腺癌细胞的侵袭;Bi kuni n具有一定的临床应用前景。

Objective To study the effects of bikunin on the invasion of PC3 prostate cancer ceils and its underlying mechanism. Methods We treated PC3 cells with bikunin and assessed its effects on cell invasion. We also detected the level of phosphorylated PI3K and AKT after bikunin treatment. Moreover, we assessed the influence of the inhibitors of PI3K and AKT on cell invasion in PC3 cells. Furthermore, we assessed the impact of constitutively active PI3K transfection on bikunin＇s activity.Results Our results revealed that bikunin treatment significantly suppressed cell invasion in PC3 cells. The activity of PI3K and AKT was also inhibited by bikunin treatment. Constitutively active PI3K transfection suppressed the inhibition of bikunin on cell invasion. Conclusion Bikunin can inhibit the invasion of PC3 cells, PI3K/AKT pathway might be involved in this process. Bikunin might be a promising therapeutic drug for prostate cancer.