Geng Chang-Xin, Zeng Zhao-Chong, Wang Ji-Yao
Director of Department of Gastroenterology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
World J Gastroenterol. 2003 Apr;9(4):696-700. doi: 10.3748/wjg.v9.i4.696.
To investigate the in vitro anti-hepatocellular carcinoma (HCC) activity of docetaxel against SMMC-7721 HCC cells and its possible mechanism.
The HCC cells were given different concentrations of docetaxel and their growth was measured by colony forming assay. Cell cycle and apoptosis were analyzed by flow cytometry and fluorescence microscopy (acridine orange/ethidium bromide double staining, AO/EB), as well as electronic microscopy. The SMMC-7721 HCC cell reactive oxygen species (ROS) and glutathione (GSH) were measured after given docetaxel.
Docetaxel inhibited the hepatocellular carcinoma cells growth in a concentration dependent manner with IC(50) 5 x 10(-10)M. Marked cell apoptosis and G2/M phase arrest were observed after treatment with docetaxel >=10(-8)M. Docetaxel promoted SMMC-7721 HCC cells ROS generation and GSH deletion.
Docetaxel suppressed the growth of SMMC-7721 HCC cells in vitro by causing apoptosis and G2/M phase arrest of the human hepatoma cells, and ROS and GSH may play a key role in the inhibition of growth and induction of apoptosis.
研究多西他赛对SMMC - 7721肝癌细胞的体外抗肝癌活性及其可能机制。
给予肝癌细胞不同浓度的多西他赛,通过集落形成试验检测其生长情况。采用流式细胞术、荧光显微镜(吖啶橙/溴化乙锭双重染色,AO/EB)以及电子显微镜分析细胞周期和凋亡情况。给予多西他赛后检测SMMC - 7721肝癌细胞的活性氧(ROS)和谷胱甘肽(GSH)水平。
多西他赛以浓度依赖性方式抑制肝癌细胞生长,IC(50)为5×10(-10)M。多西他赛≥10(-8)M处理后观察到明显的细胞凋亡和G2/M期阻滞。多西他赛促进SMMC - 7721肝癌细胞ROS生成和GSH消耗。
多西他赛通过诱导人肝癌细胞凋亡和G2/M期阻滞抑制SMMC - 7721肝癌细胞体外生长,ROS和GSH可能在抑制生长和诱导凋亡中起关键作用。