title: [Hypoxia upregulates the expression of annexin A1 in lung adenocarcinoma a549 cells].
abstract: OBJECTIVE
  The growth of tumor often faced up with lackness of blood and oxygen, and it has been reported that Annexin A1 may be involved in tumor. The aim of this investigation is to explore the characteristics of expression of Annexin A1 in lung adenocarcinoma A549 cells after hypoxia.
  
  
  METHODS
  A549 cells were exposured to either normoxia (21%O₂) or hypoxia (1%O₂) condition for 4 h, 12 h, 24 h. The expressions of Annexin A1 mRNA levels were measured by RT-PCR. The expressions of Annexin 1 protein were investigaged by Western blot. The relative content of reactive oxygen species (ROS) were assayed by special kit. The expressions of nuclear translocation of NF-κB was assayed by Western blot; After been treated with ROS scavenger NAC and PDTC, the levels of Annexin 1 protein of A549 cells were measured by Western blot.
  
  
  RESULTS
  Compared with normoxia group, the Annexin A1 mRNA in hypoxia group increased after 4 h, and then decreased gradually; Moreover, Annexin 1 protein levels of A549 cells were also increased when treated with hypoxia. An increaing of ROS production in cells exprosed to hypoxia was detected. NAC and PDTC inhibited hypoxia-induced Annexin A1 increase.
  
  
  CONCLUSIONS
  Hypoxia upregulates the expression of Annexin A1 in lung adenocarcinoma A549 cells, in which process ROS-NF-κB may paticipate in.
authors.affiliation: Department of Respiratory, Wuhan General Hospital of Guangzhou Division PLA, Wuhan 430070, China.
authors.forename: Zhenhong
authors.initials: Z
authors.lastname: Hu
authors.forename: Jian
authors.initials: J
authors.lastname: Huang
authors.forename: Zhenhua
authors.initials: Z
authors.lastname: Li
authors.forename: Xiaoxu
authors.initials: X
authors.lastname: Li
authors.forename: Zuhong
authors.initials: Z
authors.lastname: Fu
authors.forename: Haichao
authors.initials: H
authors.lastname: Liu
authors.forename: Libin
authors.initials: L
authors.lastname: Guan
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D021581:Active Transport, Cell Nucleus; D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D017305:Annexin A1 / Q000235:genetics* / Q000378:metabolism*; D000975:Antioxidants / Q000494:pharmacology; D015153:Blotting, Western; D015687:Cell Hypoxia; D045744:Cell Line, Tumor; D002467:Cell Nucleus / Q000378:metabolism; D016166:Free Radical Scavengers / Q000494:pharmacology; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D011759:Pyrrolidines / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013859:Thiocarbamates / Q000494:pharmacology; D015854:Up-Regulation
chemical_list: D017305:Annexin A1; D000975:Antioxidants; D016166:Free Radical Scavengers; D016328:NF-kappa B; D011759:Pyrrolidines; D017382:Reactive Oxygen Species; D013859:Thiocarbamates; C020972:pyrrolidine dithiocarbamic acid; D000111:Acetylcysteine