Journal of Jilin University Medicine Edition ›› 2018, Vol. 44 ›› Issue (02): 229-234.doi: 10.13481/j.1671-587x.20180205

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Regulation of Wnt5a in apoptosis of human lung adenocarcinoma A549 cells and its mechanism

YANG Yi, BAO Kangda, ZHOU Yanbing, YUAN Chao, LI Yong, LIU Xiaoming, XU Jinrui   

  1. School of Life Science, Ningxia University, Key Laboratory of Protection and Utilization of Special Biological Resources in Western China, Ministry of Education, Yinchuan 750021, China
  • Received:2017-07-01 Online:2018-03-28 Published:2018-03-30

Abstract: Objective:To investigate the regulation effect of Wnt5a on the apoptosis of lung adenocarcinoma A549 cells,and to clarify its mechanism. Methods: The human lung adenocarcinoma cells were selected.The A549 cells treated with Wnt5a were used as treatment group,and the A549 cells treated with C culture solution were used as control group.The apoptotic body induced by Wnt5a was assessed with TUNEL assay; the apoptotic rates of the A549 cells in various groups were detected by Annexin Ⅴ-FITC/PI double staining;the reactive oxygen species(ROS) levels in the A549 cells in various groups were determined with DCFH-DA fluorescence probe,and the mitochondria membrane potential was assessed with JC-1 staining method.Western blotting was used to analyze the expression levels of apoptosis-related proteins in the A549 cells in various groups. Results: Compared with control group,the apoptotic rates of the A549 cells in treatment group 12,24,and 48 h after treatment were significantly increased(P<0.01);the ROS levels were increased(P<0.05);the mitochondria membrane potentials were decreased(P<0.05),the expressing amount of BAX was up-regulated and the expression amount of AIF was down-regulated. Conclusion: Wnt5a has regulation on the apoptosis of human lung adenocarcinoma cells and can promote the apoptosis of A549 cells through mitochondrial pathway.

Key words: apoptosis, Wnt5a, reactive oxygen species, lung adenocarcinoma A549 cells, mitochondria membrane

CLC Number: 

  • R734.3