论文部分内容阅读
目的 探讨As2 O3 对人食管鳞癌细胞的效应及其作用机制。方法 用细胞学、生物化学和DNA微阵列技术分析人食管鳞癌细胞经As2 O3 处理前后细胞形态、生长状况及基因表达的改变。结果 As2 O3 可显著抑制人食管鳞癌细胞的生长 ,引起G2 /M期阻滞 ;激活半胱天冬氨酸蛋白水解酶 ;细胞发生凋亡。多数凋亡相关基因经As2 O3 诱导后表现为升调节 ,细胞周期调控蛋白和细胞内信号通路中促进细胞分裂的受体和因子的表达发生改变。结论 砷能激活蛋白水解酶 (caspases) ,或者同时引起DNA损伤 ,产生G2 /M期阻滞 ,也能诱导表达凋亡所需的蛋白 ,启动凋亡过程 ;这也表明As2 O3 对人食管鳞癌细胞的效应是广泛的 ,可能通过多个通路激活细胞凋亡 ,并引起多种类型基因表达改变。
Objective To investigate the effect of As2 O3 on human esophageal squamous cell carcinoma and its mechanism. Methods Cytology, biochemistry and DNA microarray were used to analyze the changes of cell morphology, growth and gene expression in human esophageal squamous carcinoma cells treated with As 2 O 3. Results As2 O3 could significantly inhibit the growth of human esophageal squamous cell carcinoma cells, causing G2 / M arrest; activation of caspase; and apoptosis of cells. Most apoptosis-related genes were up-regulated after As2 O3 induction, and the expression of cell cycle regulatory proteins and intracellular signal transduction promoted the division of the receptors and factors. Conclusion Arsenic can activate caspases or induce DNA damage and induce G2 / M arrest. It also induces the expression of proteins required for apoptosis and initiates the process of apoptosis. This also indicates that As 2 O 3 can inhibit the growth of human esophageal squamous cell carcinoma The effects of cancer cells are widespread and may activate apoptosis through multiple pathways and lead to altered expression of many types of genes.