摘要
目的研究激酶功能区受体(KDR)基因表达沉默后对前列腺癌PC-3细胞裸鼠体内成瘤能力的影响。方法将15只5周龄BALB/c雄性裸鼠随机分为干扰组、阴性质粒组和未转染组,每组5只。分别接种构建的pSilencer 3.1-KDR siRNA表达质粒转染PC-3细胞、阴性对照质粒pSilencer3.1-NC转染PC-3细胞以及未转染的PC-3细胞于裸鼠皮下;观察各组PC-3细胞在裸鼠体内成瘤率、瘤体生长速度以及平均瘤质量等方面的变化,RT-PCR和Western blot技术检测瘤体KDR基因和蛋白表达。结果pSilencer3.1KDR质粒转染组的裸鼠瘤体生长速度明显慢于未转染组和pSilencer3.1-NC质粒转染组;与未转染组和PSilencer3.1-NC组相比,pSilencer3.1-KDR组肿瘤的生长受到明显抑制,平均体积较小(0.28 cm3vs 0.721 cm3,0.715 cm3,P<0.01),平均瘤质量较轻(0.14 g vs 0.648 g,0.635 g,P<0.01);裸鼠肿瘤组织中KDR mRNA和蛋白的表达明显降低。结论 RNAi介导的KDR基因沉默可显著影响PC-3细胞裸鼠体内的瘤体生长速度,KDR有可能成为肿瘤治疗的新靶点。
Objective To study the change in the tumor growth of prostate cancer cell line PC-3 in nude mice xenografts after kinase domain receptor(KDR) silencing by RNA interference.Methods A total of 15 5-week-old male nude mice were randomly divided into normal PC-3 cell group(negative control),RNA interference group and pSilencer3.1-NC group,with 5 mice in every group.The nude mice were respectively treated with subcutaneous injection of 0.5 mL(2.0×107/mL) normal PC-3 cells,and the same volume of PC-3 cells transfected with pSilencer3.1-KDR and pSilencer3.1-NC vectors,respectively.By measuring the tumor volumes every 3 d and the tumor weights after 4 weeks,we recorded tumor formation rate,tumor growth rate and mean tumor weight.The expression of KDR at both mRNA and protein levels was detected by RT-PCR and Western blotting,respectively.Results Tumor growth was significantly slower in the pSilencer3.1-KDR group than in the negative control group and the pSilencer3.1-NC group.After 4 weeks,the mean volume of tumor in the pSilencer3.1-KDR group was significantly smaller than that in the other two groups(0.28 cm3 vs 0.715 cm3 and 0.721 cm3,P0.01),so was the mean weight of tumor(0.14 g vs 0.635 g and 0.648 g,P0.01).In addition,KDR mRNA and protein expressions significantly decreased.Conclusion The tumor growth in nude mice xenografts can be efficiently inhibited by KDR silencing mediated by RNAi,so the suppression of KDR expression might be a promising strategy for the treatment of human prostate cancer.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2013年第2期154-156,160,共4页
Chinese Journal of Cellular and Molecular Immunology
基金
国家自然科学基金(31172166
81171367)