title: [Methylation status and protein expression of adenomatous polyposis coli (APC) gene in breast cancer].
abstract: OBJECTIVE
  Protein expression product of adenomatous polyposis coli (APC) gene is an important component of Wnt signal transduction pathway. APC gene inactivation leads to dysfunction of beta-catenin protein degradation, and then activates Tcf/Lef and causes abnormal transcription of oncogenes, such as c-myc, c-jun and cyclin D1, finally leads to carcinogenesis. This study was to investigate the correlation of methylation status of APC gene promoter 1A to protein expression of APC gene in breast cancer, and analyze the correlation of aberrant methylation of APC gene to clinicopathologic features of breast cancer.
  
  
  METHODS
  Methylation status of APC gene promoter 1A in 76 specimens of breast cancer and corresponding adjacent tissues was detected by methylation-specific polymerase chain reaction; the expression of APC protein was detected by immunohistochemistry.
  
  
  RESULTS
  The methylation rate of APC gene promoter 1A was significantly higher in breast cancer than in pericancerous normal breast tissue (36.8% vs. 0, P < 0.05). The positive rate of APC protein was significantly lower in breast cancer than in normal breast tissue (52.4% vs. 100%, P < 0.05). The promoter methylation of APC gene was positively correlated to TNM stage (r=0.296, P < 0.05), but negatively correlated to the expression of APC protein (r=-0.368, P < 0.05).
  
  
  CONCLUSIONS
  Abnormal methylation of APC gene occurs in the progression of breast cancer, which is the main cause for the absence of APC protein expression, and the major mechanism of inactivation of APC gene.
authors.affiliation: First Department of General Surgery, Shengjing Hospital, China Medical University, Shenyang, Liaoning 110004, P. R. China. liuzhen7099@vip.sina.com
authors.forename: Zhen
authors.initials: Z
authors.lastname: Liu
authors.forename: Lei
authors.initials: L
authors.lastname: Yang
authors.forename: Dong-Xu
authors.initials: DX
authors.lastname: Cui
authors.forename: Bao-Lin
authors.initials: BL
authors.lastname: Liu
authors.forename: Xiao-Bo
authors.initials: XB
authors.lastname: Zhang
authors.forename: Wen-Feng
authors.initials: WF
authors.lastname: Ma
authors.forename: Qiang
authors.initials: Q
authors.lastname: Zhang
mesh_terms: D025601:Adenomatous Polyposis Coli Protein / Q000235:genetics / Q000378:metabolism*; D000328:Adult; D000368:Aged; D001940:Breast / Q000378:metabolism; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D018270:Carcinoma, Ductal, Breast / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D002285:Carcinoma, Intraductal, Noninfiltrating / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D018275:Carcinoma, Lobular / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D018899:CpG Islands; D019175:DNA Methylation; D005260:Female; D017491:Genes, APC; D006801:Humans; D008207:Lymphatic Metastasis; D008875:Middle Aged; D009367:Neoplasm Staging; D011401:Promoter Regions, Genetic
chemical_list: D025601:Adenomatous Polyposis Coli Protein