丙戊酸诱导前列腺癌自噬并促进SPARCL1蛋白的表达  

Valproic acid induces autophagy and regulates the expression of SPARCL1 protein in prostate cancer cells

作　　者：郑懿[1] 蒋伟[1] 金讯波[1] 王慕文[1] 张沂南[1] 夏庆华[1] 

机构地区：[1]山东大学附属省立医院泌尿微创科,济南250021

出　　处：《山东大学学报（医学版）》2013年第7期32-35,41,共5页Journal of Shandong University:Health Sciences

基　　金：山东省科技厅立项项目(BS2010YY047)

摘　　要：目的通过对丙戊酸(VPA)诱导前列腺癌发生自噬现象的观测及对SPARCL1蛋白表达的调节作用,探讨VPA对前列腺癌细胞抑制作用的可能机制。方法选取3种常见前列腺癌细胞系PC3、DU145和LNCaP,经过不同浓度VPA处理,计算VPA对细胞的抑制率,采用透射电镜观察自噬的特异性超微结构,Western Blotting技术检测自噬特异性蛋白LC3-Ⅱ和Beclin-1以及SPARCL1蛋白的表达。结果 3组前列腺癌细胞系经过药物处理后,均产生抑制作用(P<0.05),且呈药物浓度相关性。自噬蛋白的表达随药物浓度的提高而增加(P<0.05)。VPA还能诱导肿瘤细胞分泌SPARCL1蛋白。结论 VPA可使前列腺癌细胞发生自噬并调节SPARCL1表达,这可能是其发挥抗肿瘤作用的重要原因。Objective To observe the autophagy and regulation of SPARCL1 protein in prostate cancer cells induced by valproic acid （VPA） and to explore the further antitumor mechanism. Methods After treatment with VPA, PC3, DU145 and LNCaP prostate cancer cells were examined for the inhibition rate. Autophagy markers LC3-Ⅱ, Beclin-1 and SPARCL1 protein expressions were examined by Western blotting. The specific organelle structure was detected by electron microscope. Results After treated by VPA, the inhibition rate increased （ P 〈 0.05 ）, as confirmed by detec- tion of increasing LC3- Ⅱ and Beclin-1 expressions in VPA-treated samples （ P 〈 0.05 ）. SPARCL1 protein also showed significant increase after treatment with VPA （ P 〈 0.05 ）. Conclusion VPA showed an antitumor effect by inducing autophagy and secretion of SPARCL1 protein in the human prostate cancer cell model.

关 键 词：丙戊酸 前列腺肿瘤 自噬 SPARCL1蛋白 

分 类 号：R697[医药卫生—泌尿科学]