中文摘要：

8-氯-腺苷（8-Cl-adenosine，8-Cl-Ado）可诱导人非小细胞性肺癌细胞H1299发生凋亡，但其分子机制还没有阐明.首先用四唑盐（MTT）比色法检测了8-Cl-Ado对H1299细胞的生长抑制作用.进一步采用蛋白质免疫印迹法（Western blotting）检测了8-Cl-Ado处理H1299细胞后，procaspase-3的激活情况以及E2F1的蛋白水平.通过用pcDNA-HA-E2F1表达载体和pSUPER-E2F1 RNA干扰载体分别转染H1299细胞，研究在E2F1过表达和RNA干扰（RNAinterference，RNAi）两种情况下对凋亡的影响.实验结果表明，8-Cl-Ado可抑制H1299细胞的生长，激活凋亡关键执行蛋白procaspase-3，升高E2F1蛋白水平.当E2F1过表达后，同时伴有procaspase-3的激活，而E2F1表达受到抑制后，与对照相比，8-Cl-Ado引起的procaspase-3的激活被明显抑制，说明E2F1介导8-Cl-Ado引起的人肺癌细胞H1299的凋亡.

英文摘要：

In this article,we intend to investigate the mechanism of 8-Cl-adenosine（8-Cl-Ado）-induced apoptosis in human non-small cell lung carcinoma H1299 cells.MTT assay was first employed to determine the anti-proliferation effects of 8-Cl-Ado;Western blotting was used to examine the activation of procaspase-3 and the levels of E2F1 after 8-Cl-Ado exposures.After transfecting pcDNA-HA-E2F1（E2F1 overexpression） or pSUPER-E2F1（RNAi of E2F1） vector into H1299 cells,the procaspase-3,as a marker of apoptotic cell death,as well as E2F1 was determined by Western blotting.The results showed that 8-Cl-Ado induced growth inhibition in H1299 cells,by the activation of procaspase-3 and the up-regulation of E2F1.Procaspase-3 was activated in response to E2F1 over-expression,and markedly inhibited following E2F1 knocke-down by RNAi.Our data suggested that E2F1 mediated 8-Cl-Ado-induced apoptosis in human lung cancer cells H1299.