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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 investigate the possible mechanism of VPA inhibition on prostate cancer cells by observing autophagy induced by valproic acid (VPA) and regulating the expression of SPARCL1 protein. Methods Three common prostate cancer cell lines, PC3, DU145 and LNCaP, were selected and treated with different concentrations of VPA to calculate the inhibitory rate of VPA. The autophagic specific ultrastructure was observed by transmission electron microscopy and the autophagy specificity was detected by Western Blotting Protein LC3-II and Beclin-1 and SPARCL1 protein expression. Results All three groups of prostate cancer cell lines were inhibited by drugs (P <0.05), and showed drug concentration dependence. The expression of autophagy increased with the increase of drug concentration (P <0.05). VPA can also induce tumor cells to secrete SPARCL1 protein. Conclusion VPA can induce autophagy in prostate cancer cells and regulate the expression of SPARCL1, which may be an important reason for its anti-tumor effect.