title: Activation of aryl hydrocarbon receptor suppresses invasion of esophageal squamous  cell carcinoma cell lines.
abstract: OBJECTIVE
  Esophageal cancer is the eighth most common malignancy and sixth leading cause of cancer deaths in the world. Recent studies have shown the potential role of the aryl hydrocarbon receptor (AhR) in tumor development; however, little is known about its role in esophageal squamous cell carcinoma. In the present study, we evaluated AhR expression in esophageal tumor tissues as well as cell lines and investigated the effects of AhR activation by its agonist BNF on esophageal squamous cell carcinoma invasion using Eca109 and TE-13 cells as a model.
  
  
  METHODS
  Western blotting was performed to detect the AhR and CYP1A1 protein expression. Transwell migration assays were carried out to study the effects of BNF on esophageal squamous cell carcinoma cell invasion. AhR-specific siRNA was used to knock down the expression of AhR protein.
  
  
  RESULTS
  Our results showed that AhR was highly expressed in esophageal squamous cell carcinoma tissues and cell lines when compared with its expression in normal tissue. AhR siRNA robustly decreased AhR protein expression in both Eca109 and TE-13 cells. BNF significantly inhibited invasion of human esophageal squamous cell carcinoma cells via activation of AhR.
  
  
  CONCLUSIONS
  The obtained results provide critical information on the roles of BNF in mediating esophageal squamous cell carcinoma invasion. This information could be useful for future therapeutic intervention in this lethal human disease.
authors.affiliation: Interventional Oncology Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, PR China.
authors.forename: Jianhao
authors.initials: J
authors.lastname: Zhang
authors.forename: Hong
authors.initials: H
authors.lastname: Zong
authors.forename: Shenglei
authors.initials: S
authors.lastname: Li
authors.forename: Dandan
authors.initials: D
authors.lastname: Zhang
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Qingxin
authors.initials: Q
authors.lastname: Xia
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D015153:Blotting, Western; D002294:Carcinoma, Squamous Cell / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D045744:Cell Line, Tumor; D019363:Cytochrome P-450 CYP1A1 / Q000032:analysis / Q000037:antagonists & inhibitors; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D004938:Esophageal Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D015971:Gene Expression Regulation, Enzymologic; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D009361:Neoplasm Invasiveness; D018336:Receptors, Aryl Hydrocarbon / Q000187:drug effects / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D019324:beta-Naphthoflavone / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; D004791:Enzyme Inhibitors; D018336:Receptors, Aryl Hydrocarbon; D019324:beta-Naphthoflavone; C569463:CYP1A1 protein, human; D019363:Cytochrome P-450 CYP1A1