用基因芯片研究尼古丁对肺腺癌细胞凋亡基因表达的影响

目的：探讨尼古丁对人肺癌细胞生长的影响及其机制。方法：采用MTT法分析尼古丁处理人肺腺癌细胞SPC-A后生长变化；采用基因芯片技术检测尼古丁处理SPC-A-1细胞前后，细胞凋亡相关基因表达的变化。结果：尼古丁对SPC-A细胞的生长具有显著的促进作用，但随着尼古丁浓度的增大，促进作用也下降。100 μg/L尼古丁处理后，SPC-A-1细胞451个凋亡相关基因中有显著变化的基因有80个，其中，促进凋亡相关基因上调的有 29 个，下调的有13 个；抑制凋亡相关基因上调的有26个，下调的有12个。结论：尼古丁能促进人肺腺癌细胞生长，调节许多凋亡相关基因表达。

Effect of nicotine in vitro on expressions of apoptosis-related genes in human lung adenocarcinoma cells by cDNA microarray

AIM: To investigate effect of nicotine on growth of human lung adenocarnoma cells and expressions of apoptosis-related gene. METHODS: Lung adenocarcinoma cell line, SPC-A-1, was cultured in the presence of various concentrations (1-1 000 μg/L) of nicotine for 48 hours. MTT was applied to evaluate effect of nicotine in vitro on growth of SPC-A-1 cell line. After SPC-A-1 cells were treated with 100 μg/L for 48 hours, cDNA expression profile microarray was used to detect the expressions of 451 apoptosis-related genes in SPC-A-1 cell line. RESULTS: Significant proliferation in SPC-A-1 cells treated with nicotine (1-10 μg/L) was observed, but this effect decreased with increase in concentration of nicotine in culture. Growth inhibition rate of 1, 10, 100, 1 000 μg/L of nicotine was 27%, -40%, -40% and -93%. Microarray detection showed that significantly different expressions appeared in 80 of 451 apoptosis-related genes. 29 apoptosis-promoted genes and 26 apoptosis-inhibited genes were up-regulated significantly (CY3/CY5>2.0), and 25 genes were significantly down-regulated (CY3/CY5<0.5). CONCLUSION: Nicotine may promote growth of human lung adenocarcinoma cell through regulating many apoptosis-related gene expressions.