槚如酸对雄激素非依赖型前列腺癌细胞株Du145的作用和对COX2、C—myc、VEGFA表达的影响及意义

Anacardic acid induces apoptosis of prostate cancer Du145 cells through inhibiting expression of COX2, C-myc and VEGFA

目的探讨药物板如酸对雄激素非依赖型前列腺癌细胞株Dul45的抗肿瘤作用及对癌基因COX2、C-myc、VEGFA表达的影响及意义。方法培养Du145细胞株，使用MTT法测定不同浓度板如酸对Dul45细胞增殖的影响，获得药物最佳作用时间和剂量；使用流式细胞仪检测掼如酸对Dul45细胞周期的影响和对细胞凋亡的作用；并通过RT—PCR及Westernblot来测定板如酸对Dul45细胞内癌基因C．myc、COX2、VEGFA的mRNA和蛋白表达的影响。结果桢如酸抑制Dul45细胞增殖，其作用具有剂量、时间效应关系；根如酸诱导Dul45细胞凋亡，并阻滞细胞周期于G1／s期；槚如酸处理后，Dul45细胞株内癌基因COX2、C-myc、VEGFA的mRNA和蛋白表达均降低。结论桢如酸对雄激素非依赖型前列腺癌Dul45细胞具致死作用，其抗癌机制值得进一步探讨。

Objective To investigate the biological effect of anacardic acid on androgen independent prostate cancer cells Du145 cells and its possible mechanism. Methods Growths of Du145 cells in exposure to different concentration of anacardic acid were analyzed using MTT assay to determine the optimal dose and action time ofanacardic acid Apoptosis rate and cell cycle of Dul45 cells treated with anacardic acid were examined by flow cytometry. The expressions of C-myc, VEGFA and COX2 were detected by RT - PCR and Western Blot, respectively. Results Cell proliferation was inhibited under treatment of anacardic acid, cell cycle G1/S arrest and apoptosis of Du145 cells were induced,, and the expressions of COX2, C-myc and VEGFA in Du145 cells were decreased obviously. Conclusion Anacardic acid showed an obvious antitumor activity on Du145 cells and its possible mechanism merited further investigation.