The effect of PIM-1 silence on the growth of human prostate cancer xenograft tumor in nude mice / 天津医药

ABSTRACT

Objective To study the effect of PIM-1 gene silence by RNA interference (RNAi) on the growth of human prostate cancer xenograft tumor in nude mice. Methods The xenograft tumor model of human prostate cancer was established by injecting PC-3 cells in armpits of 12 nude mice. After modeling, the nude mice were randomly divided into three groups interference plasmid group (injecting with RNAi recombinant plasmid), empty plasmid group and negative control group (liposome every), 4 mice in each group. Mice were injected every 2 days for 5 times. The tumor volumes of xenografts were measured during experiment, and the curve of tumor growth was drawn accordingly. The quality of tumor was measured, and the inhibitory rate of tumor was calculated at the end of the experiments. The expression levels of PIM-1, c-MYC mRNA and protein in xenograft tumors were detected by real-time PCR and Western blot assay, respectively. Furthermore, immunohistochemistry staining was used to verify the expression of PIM-1. Results The xenograft tumor model of human prostate cancer was established successfully. The volume of tumor was significantly decreased 6 days after the injection treatment in interference plasmid group than that of empty plasmid group and negative control group. The effect of suppressing tumor growth was remarkable. The expression levels of PIM-1 mRNA and protein were down-regulated significantly in interference plasmid group than those of other two groups. The immunohistochemical staining of PIM-1 showed the same changes. There was no significant difference in c-MYC protein level between the three groups. But interestingly, the c-MYC mRNA level was significantly decreased in interference plasmid group than that of other two groups. Conclusion The silence of PIM-1 gene by RNAi recombinant plasmid can result a significant growth suppression of the human prostate cancer xenograft tumors in nude mice. The expression of c-MYC gene is down-regulated at translation level in the therapeutic group concomitantly. PIM-1 may be a promising target of gene therapy for prostate cancer.