title: KAI1, CAR, and Smad4 expression in the progression of colorectal tumor.
abstract: OBJECTIVE
  The abnormal expression of several genes is involved in the development of colorectal tumors. The aim of this study was to examine the expression of KAI1, CAR, and Smad4, which has been associated with the progression of other cancers.
  
  
  METHODS
  We examined 12 adenomas, 38 primary carcinomas, 10 liver metastases, and 7 adenocarcinoma cell lines, by fluorescent multiplex reverse transcription-polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  KAI1 expression was higher in adenomas (2.55 +/- 0.61; P < 0.05) and primary carcinomas (3.30 +/- 0.42; P < 0.005) than in normal mucosa, but it was not correlated with tumor stage. CAR expression was lower in Dukes' B (1.28 +/- 0.53) than in Dukes' A (2.38 +/- 0.48) (P < 0.05), but increased with tumor progression; Dukes' C (1.45 +/- 0.25), Dukes' D (1.53 +/- 0.14), and metastases (2.09 +/- 0.39) (P < 0.05). Smad4 expression increased in adenomas (2.30 +/- 0.46; P < 0.05), but decreased with tumor progression; Dukes' A (2.14 +/- 0.37), Dukes' B (1.65 +/- 0.41), Dukes' C (1.57 +/- 0.25), Dukes' D (1.08 +/- 0.18), and metastases (0.82 +/- 0.21) (P < 0.05).
  
  
  CONCLUSIONS
  These results suggest that the upregulation of CAR and down-regulation of Smad4 are associated with the progression of colorectal tumors, while the upregulation of these genes and of KAI1 seems to be involved in the early stage.
authors.affiliation: First Department of Internal Medicine, Hirosaki University School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Mikami
authors.forename: K
authors.initials: K
authors.lastname: Ookawa
authors.forename: T
authors.initials: T
authors.lastname: Shimoyama
authors.forename: S
authors.initials: S
authors.lastname: Fukuda
authors.forename: H
authors.initials: H
authors.lastname: Saito
authors.forename: A
authors.initials: A
authors.lastname: Munakata
mesh_terms: D000074183:ATPases Associated with Diverse Cellular Activities; D015703:Antigens, CD; D015815:Cell Adhesion Molecules / Q000032:analysis*; D015179:Colorectal Neoplasms / Q000737:chemistry / Q000473:pathology*; D004268:DNA-Binding Proteins / Q000032:analysis*; D018450:Disease Progression; D004586:Electrophoresis; D005453:Fluorescence; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D051861:Kangai-1 Protein; D008113:Liver Neoplasms / Q000737:chemistry / Q000473:pathology* / Q000556:secondary; D008562:Membrane Glycoproteins / Q000032:analysis*; D008666:Metalloendopeptidases; D009154:Mutation; D011518:Proto-Oncogene Proteins; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051901:Smad4 Protein; D015534:Trans-Activators / Q000032:analysis*
chemical_list: D015703:Antigens, CD; C497688:CD82 protein, human; D015815:Cell Adhesion Molecules; D004268:DNA-Binding Proteins; D051861:Kangai-1 Protein; D008562:Membrane Glycoproteins; D011518:Proto-Oncogene Proteins; C497796:SMAD4 protein, human; D051901:Smad4 Protein; D015534:Trans-Activators; D008666:Metalloendopeptidases; C112889:SPG7 protein, human; D000074183:ATPases Associated with Diverse Cellular Activities