title: Down-regulation of gut-enriched Kruppel-like factor expression in esophageal cancer.
abstract: OBJECTIVE
  Esophageal carcinoma is one of the most common malignant tumors in China. But the molecular mechanisms of esophageal carcinoma remains unclear. Gut-enriched Kruppel-like factor (GKLF) is a newly identified transcription factor which is expressed abandantly in the epithelial cells of the gastrointestinal tract and deregulation of GKLF was linked to several types of cancer. It is of interest to study the expression and role of GKLF in esophageal carcinoma.
  
  
  METHODS
  Semi-quantitative RT-PCR was used to compare GKLF expression in esophageal squamous cell carcinoma to normal mucosa of the same patients. The serum deprivation inducibility of GKLF was observed in an esophageal squamous cancer cell line by comparison to the primary culture of human fibroblast. The effect of antisense GKLF transfection on the proliferation and adhesion of esophageal squamous cancer cell line was also observed.
  
  
  RESULTS
  The level of GKLF transcript is lower in esophageal squamous cell carcinoma compared to paired normal-appearing mucosa in 14 of 17 of the tumors analyzed. The serum deprivation inducibility of GKLF was greatly decreased in an esophageal squamous cancer cell line compared to the primary culture of human fibroblast. Decreased expression of GKLF in the esophageal cancer cell by antisense GKLF transfection increased its proliferation rate compared with that of vector transfected cell control (P<0.05). Transfection of antisense GKLF decreased its adhesion ability (P<0.05).
  
  
  CONCLUSIONS
  The findings of this study demonstrate the down-regulation of GKLF in esophageal squamous cancer, and suggest that deregulation of GKLF may play a role in initiation and/or progression as well as the metastasis of esophageal squamous cancer.
authors.affiliation: National Laboratory of Molecular Oncology, Cancer Institute, Chinese Academy of Medical Sciences, Beijing 100021, China.
authors.forename: Nan
authors.initials: N
authors.lastname: Wang
authors.forename: Zhi-Hua
authors.initials: ZH
authors.lastname: Liu
authors.forename: Fang
authors.initials: F
authors.lastname: Ding
authors.forename: Xiu-Qin
authors.initials: XQ
authors.lastname: Wang
authors.forename: Chuan-Nong
authors.initials: CN
authors.lastname: Zhou
authors.forename: Min
authors.initials: M
authors.lastname: Wu
mesh_terms: D000818:Animals; D001483:Base Sequence; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000473:pathology; D002448:Cell Adhesion; D002455:Cell Division; D002478:Cells, Cultured; D016895:Culture Media, Serum-Free; D018076:DNA, Complementary / Q000235:genetics; D004273:DNA, Neoplasm / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics*; D015536:Down-Regulation; D004938:Esophageal Neoplasms / Q000235:genetics* / Q000473:pathology; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D000090062:Kruppel-Like Factor 4; D051741:Kruppel-Like Transcription Factors; D051379:Mice; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014157:Transcription Factors / Q000235:genetics*; D014162:Transfection; D014407:Tumor Cells, Cultured
chemical_list: D016895:Culture Media, Serum-Free; D018076:DNA, Complementary; D004273:DNA, Neoplasm; D004268:DNA-Binding Proteins; C000715467:KLF4 protein, human; C000715468:Klf4 protein, mouse; D000090062:Kruppel-Like Factor 4; D051741:Kruppel-Like Transcription Factors; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D014157:Transcription Factors