解剖学报

›› 2011, Vol. 42 ›› Issue (1): 50-53.doi: 10.3969/j.issn.0529-1356.2011.01.009

• 论著 • 上一篇    下一篇

阿糖胞苷诱导肺腺癌细胞凋亡与p73激活相关

张露1 ;刘宁1 ;吕丹瑜1 ;马万云2 ;李英1 *   

  1. 1. 北京大学基础医学院人体解剖学与组织学胚胎学系，100191 北京; 2. 清华大学物理系原子分子纳米科学教育部重点实验室， 北京 100191
  • 收稿日期:2010-04-16 修回日期:2010-05-05 出版日期:2011-01-06
  • 通讯作者: 李英

p73 activation is involved in regulation of Ara-C-induced apoptosis in human lung adenocarcinoma cells

  1. 1. Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing 100083 China;2. Key Laboratory for Atomic and Molecular Nanosciences of the Ministry of Education, Department of Physics, Tsinghua University, Beijing 100191, China
  • Received:2010-04-16 Revised:2010-05-05 Online:2011-01-06
  • Contact: LI Ying

关键词: 阿糖胞苷, p73, p53, A549细胞, TUNEL法, 透射电镜, 免疫印迹法

Abstract: Objective To study the apoptosis pathway of human lung adenocarcinoma cell line A549 induced by 1-β-D-arabinofuranosylcytosine (Ara-C) EM>in vitro/EM>. Methods A549 cells were incubated with Ara-C for 72hours EM>in vitro/EM>. Biological changes of apoptotic cells were studied by TUNEL staining. Morphological changes of the A549 cells treated with Ara-C were observed by transmission electron microscope. The expressions of p53 and p73 were investigated by Western blotting. Results 1.Apoptotic rates of A549 cells exposure to Ara-C studied by TUNEL staining were higher than that of the control (EM>P/EM><0.01). 2.Apoptosis body was apparently observed by transmission electron microscope. 3.Endogenous p73 but not p53 was induced and activated in dose-dependent manner upon Ara-C treatment by Western blotting. Conclusion Ara-C can effectively induce apoptosis of A549 cells. DNA damage-induced apoptosis of A549 cells treated by Ara-C is independent of functional p53-Up-regulation of p73 may play an important role that enhances the sensitivity of A549 cells to Ara-C and be p

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