title: [Celecoxib induces apoptosis and inhibits angiogenesis in gastric cancer].
abstract: OBJECTIVE
  The aim of this study was to explore the effect of celecoxib, a cyclooxygenase-2 inhibitor, on induction of apoptosis and inhibition of angiogenesis in gastric cancer.
  
  
  METHODS
  Fifty nine gastric cancer patients were randomly divided into 2 groups: celecoxib group (n = 37) and control group (n = 22). The patients in the celecoxib group were treated orally with celecoxib 200 mg twice daily for 7 days before resection. The patients in the control group received surgical resection alone. Another group of 20 healthy subjects were recruited as normal control. The number of apoptotic tumor cells was measured by terminal deoxynucleotidyl transferse-mediated dUTP nick end labeling (TUNEL). The expression of COX-2, VEGF and the microvessel density (MVD) were evaluated by immunohistochemistry.
  
  
  RESULTS
  The TUNEL results showed an increase of apoptosis in the tumor cells after celecoxib treatment in comparison with that in the control group (7.1% +/- 1.0% vs. 6.2% +/- 0.9%, P < 0.05). The expression level of COX-2 and VEGF in the gastric cancer tissues was significantly decreased in the celecoxib group compared with those in the control group (P < 0.05). Furthermore, MVD was also significantly lower in the celecoxib group when compared with that in the control group (30.48 +/- 5.02 vs. 38.98 +/- 4.58, P < 0.05).
  
  
  CONCLUSIONS
  Oral intake of celecoxib can induce apoptosis and suppress angiogenesis in gastric cancer. It may become an effective agent in the treatment of gastric cancer.
authors.affiliation: Department of Gastroenterology, The First Hospital, Lanzhou University, Lanzhou 730000, China.
authors.forename: Jun-tao
authors.initials: JT
authors.lastname: Ran
authors.forename: Yong-ning
authors.initials: YN
authors.lastname: Zhou
authors.forename: Cheng-wei
authors.initials: CW
authors.lastname: Tang
authors.forename: Jian-rong
authors.initials: JR
authors.lastname: Lu
authors.forename: Jing
authors.initials: J
authors.lastname: Wu
authors.forename: Hong
authors.initials: H
authors.lastname: Lu
authors.forename: Guo-dong
authors.initials: GD
authors.lastname: Yang
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology; D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000187:drug effects*; D000068579:Celecoxib; D051546:Cyclooxygenase 2 / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D005260:Female; D006801:Humans; D008297:Male; D055806:Microvessels / Q000473:pathology / Q000648:ultrastructure; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000517:prevention & control*; D011720:Pyrazoles / Q000494:pharmacology* / Q000627:therapeutic use; D013274:Stomach Neoplasms / Q000378:metabolism / Q000473:pathology*; D013449:Sulfonamides / Q000494:pharmacology* / Q000627:therapeutic use; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D011720:Pyrazoles; D013449:Sulfonamides; D042461:Vascular Endothelial Growth Factor A; D051546:Cyclooxygenase 2; D000068579:Celecoxib