论文部分内容阅读
目的探查干扰素λ诱导人食管癌YES5和T.Tn细胞抗增殖的机制。方法流式细胞术检测细胞周期,膜联蛋白Ⅴ(annexinⅤ)和PI双染检测凋亡,Western印迹检测凋亡蛋白的表达。结果干扰素λ诱导人食管癌YES5和T.Tn细胞的亚G1期(sub-G1)升高,干扰素λ处理细胞与膜联蛋白Ⅴ的结合增加,干扰素λ可诱导细胞内半胱天冬酶(caspase)3的剪切,caspase抑制剂可减少干扰素λ诱导的sub-G1期升高。结论干扰素λ可诱导人食管癌YES5和T.Tn细胞发生凋亡。
Objective To investigate the mechanism of interferon λ induced anti-proliferation in human esophageal carcinoma YES5 and T.Tn cells. Methods Cell cycle was detected by flow cytometry. Apoptosis was detected by annexin Ⅴ and PI double staining. Western blotting was used to detect the expression of apoptosis protein. Results Interferon λ induced elevated sub-G1 (sub-G1) expression in human esophageal carcinoma YES5 and T. tn cells, increased binding of interferon λ-treated cells to annexin Ⅴ, and interferon λ induced intracellular caspase Caspase 3 cleavage and caspase inhibitors reduce the increase in sub-G1 phase induced by interferon-gamma. Conclusion Interferon λ can induce the apoptosis of human esophageal carcinoma YES5 and T.Tn cells.