Laboratory Medicine ›› 2015, Vol. 30 ›› Issue (5): 507-511.DOI: 10.3969/j.issn.1673-8640.2015.05.022

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Influence of 5-Aza-CdR on the apoptosis of lung cancer A549 cell and the expression of FANCF gene

YU Zongtao1, ZHANG Jicai1, GAO Qiong2, GAO Bo1, HU Chunhui1   

  1. 1. Department of Clinical Laboratory, Taihe Hospital, Hubei University of Medicine, Hubei Shiyan 442000, China
    2. Department of Respiratory Medicine, Taihe Hospital, Hubei University of Medicine, Hubei Shiyan 442000, China
  • Received:2014-06-11 Online:2015-05-30 Published:2015-06-17

Abstract: Objective To investigate the influence of 5-Aza-2'-deoxycytidine(5-Aza-CdR) on the apoptosis of lung cancer A549 cell and the expression of Fanconi anemia complementation group F(FANCF) gene. Methods A549 cells were treated with 5-Aza-CdR(0.5, 5 and 50 μmol/L, respectively). The growth of A549 cells was observed by 3-(4,5-dimethylthiazol)-3,5-diphenyltetrazolium bromide(MTT) assay. The methylation status of FANCF gene was observed by methylation specific polymerase chain reaction(PCR). The expression of FANCF mRNA was observed by fluorescence quantitation PCR. The apoptosis rate of A549 cells was analyzed by flow cytometry. Results A549 cells treated with 5-Aza-CdR displayed a slow growth. The rate of cell proliferation inhibiting (CPIR) for A549 cells changed with the concentration and treatment time of 5-Aza-CdR (P<0.005, P<0.001). FANCF mRNA expression increased after treatmert. The apoptosis rates after treatment had a positive correlation with 5-Aza-CdR dose (r=0.998, P<0.05). Conclusions 5-Aza-CdR can induce the apoptosis of A549 cells by inducing demethylation and thereby enchancing FANCF gene, enhancing tumor suppressor function, but it can increase the risk of resistance to cisplatin.

Key words: Fanconi anemia complementation group F gene, Methylation, 5-Aza-2'-deoxycytidine, A549 cell, Apoptosis

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