Hong-Bing Ma, Shan Huang, Xiao-Ran Yin, Yang Zhang, Department of Radiotherapy of Tumor Hospital, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
World J Gastroenterol. 2014 Jan 7;20(1):193-203. doi: 10.3748/wjg.v20.i1.193.
To investigate the effects of diallyl trisulfide (DATS), a garlic-derived organosulfur compound, in pancreatic cancer cells.
Human pancreatic cancer cells with wild-type p53 gene (Capan-2) and normal pancreatic epithelial cells (H6C7) were cultured in RPMI1640. DATS was prepared at a concentration of 100 μmol/L. Cell viability was determined via the methyl thiazolyl tetrazolium assay. Apoptotic cells were detected by TUNEL assay. Cell cycle analysis was performed using flow cytometry. Protein expression was determined by Western blot. Bax and Bcl-2 expression was detected by immunofluorescence. Apoptosis genes and cell cycle were assessed by quantitative real-time polymerase chain reaction.
DATS suppressed the viability of cultured human pancreatic cancer cells (Capan-2) by increasing the proportion of cells in the G2/M phase and induced apoptotic cell death. Western blot analysis indicated that DATS enhanced the expression of Fas, p21, p53 and cyclin B1, but downregulated the expression of Akt, cyclin D1, MDM2 and Bcl-2. DATS induced cell cycle inhibition which was correlated with elevated levels of cyclin B1 and p21, and reduced levels of cyclin D1 in Capan-2 cells and H6C7 cells. DATS-induced apoptosis was markedly elevated in Capan-2 cells compared with H6C7 cells, and this was correlated with elevated levels of cyclin B1 and p53, and reduced levels of Bcl-2. DATS-induced apoptosis was correlated with down-regulation of Bcl-2, Akt and cyclin D1 protein levels, and up-regulation of Bax, Fas, p53 and cyclin B protein levels in Capan-2 cells.
DATS induces apoptosis of pancreatic cancer cells (Capan-2) and non-tumorigenic pancreatic ductal epithelial cells (H6C7).
研究大蒜衍生的有机硫化合物二烯丙基三硫（DATS）对胰腺癌细胞的作用。
在 RPMI1640 中培养具有野生型 p53 基因（Capan-2）的人胰腺癌细胞和正常胰腺上皮细胞（H6C7）。将 DATS 制备成 100μmol/L 的浓度。通过噻唑蓝比色法测定细胞活力。通过 TUNEL 检测凋亡细胞。通过流式细胞术进行细胞周期分析。通过 Western blot 测定蛋白表达。通过免疫荧光检测 Bax 和 Bcl-2 的表达。通过实时定量聚合酶链反应评估凋亡基因和细胞周期。
DATS 通过增加 G2/M 期细胞的比例抑制培养的人胰腺癌细胞（Capan-2）的活力，并诱导凋亡性细胞死亡。Western blot 分析表明，DATS 增强了 Fas、p21、p53 和细胞周期蛋白 B1 的表达，但下调了 Akt、细胞周期蛋白 D1、MDM2 和 Bcl-2 的表达。DATS 诱导的细胞周期抑制与 Capan-2 细胞和 H6C7 细胞中细胞周期蛋白 B1 和 p21 的水平升高以及细胞周期蛋白 D1 水平降低有关。与 H6C7 细胞相比，DATS 在 Capan-2 细胞中诱导的细胞凋亡明显增加，这与细胞周期蛋白 B1 和 p53 水平升高以及 Bcl-2 水平降低有关。DATS 诱导的细胞凋亡与 Bcl-2、Akt 和细胞周期蛋白 D1 蛋白水平下调以及 Bax、Fas、p53 和细胞周期蛋白 B 蛋白水平上调有关。
DATS 诱导胰腺癌细胞（Capan-2）和非肿瘤性胰腺导管上皮细胞（H6C7）凋亡。
