title: Increased expression of RelA/nuclear factor-kappa B protein correlates with colorectal tumorigenesis.
abstract: OBJECTIVE
  To identify the role of RelA/nuclear factor-kappa B, an important inhibitor of apoptosis in colorectal tumorigenesis, we examined the expression of RelA in normal colorectal mucosa (n = 10), colorectal adenomas (n = 30) and colorectal adenocarcinomas (n = 30). Furthermore, the association of RelA expression with tumor cell apoptosis, proliferation, and expression of Bcl-2/Bcl-x(L )was also studied.
  
  
  METHODS
  Paraffin sections were stained with monoclonal antibodies directed against RelA, Bcl-2, Bcl-x(L), and Ki-67 to assess protein expression patterns in normal, adenomatous and colon cancer tissue. Apoptotic cells were detected by terminal deoxynucleotidyl-transferase-mediated dUTP-biotin nick end labeling (TUNEL) using an in situ detection kit.
  
  
  RESULTS
  The results of immunohistochemical staining revealed that expression of RelA, Bcl-2, Bcl-x(L), and Ki-67 labeling index (LI) significantly increased in the transition from adenoma with low dysplasia to adenocarcinoma. This transition was associated with a significant decrease in the apoptotic index (AI) and a significant increase in the Ki-67 LI. The expression of RelA correlated inversely with the AI and correlated positively with the expression of Bcl-2, Bcl-x(L), and Ki-67 LI in the transition from low-grade dysplasia to adenocarcinoma.
  
  
  CONCLUSIONS
  Our results suggest that increased expression of RelA/nuclear factor-kappa B plays an important role in the transition from colorectal adenoma with low-grade dysplasia to adenocarcinoma in the pathogenesis of colon cancer in humans.
authors.affiliation: Department of Gastroenterology, Renmin Hospital, Wuhan University, Wuhan, China.
authors.forename: Hong-Gang
authors.initials: HG
authors.lastname: Yu
authors.forename: Liang-Liang
authors.initials: LL
authors.lastname: Yu
authors.forename: Yanning
authors.initials: Y
authors.lastname: Yang
authors.forename: He-Sheng
authors.initials: HS
authors.lastname: Luo
authors.forename: Jie-Ping
authors.initials: JP
authors.lastname: Yu
authors.forename: Juris J
authors.initials: JJ
authors.lastname: Meier
authors.forename: Henning
authors.initials: H
authors.lastname: Schrader
authors.forename: Andreas
authors.initials: A
authors.lastname: Bastian
authors.forename: Wolfgang E
authors.initials: WE
authors.lastname: Schmidt
authors.forename: Frank
authors.initials: F
authors.lastname: Schmitz
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology; D000236:Adenoma / Q000378:metabolism* / Q000473:pathology; D002455:Cell Division; D002471:Cell Transformation, Neoplastic; D015179:Colorectal Neoplasms / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D007413:Intestinal Mucosa / Q000378:metabolism; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism*; D016612:Paraffin Embedding; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051996:Transcription Factor RelA; D051020:bcl-X Protein
chemical_list: C494811:BCL2L1 protein, human; D019394:Ki-67 Antigen; D016328:NF-kappa B; D019253:Proto-Oncogene Proteins c-bcl-2; D051996:Transcription Factor RelA; D051020:bcl-X Protein