[Wif-1 methylation and β-catenin expression in colorectal serrated lesions]

Zhonghua Bing Li Xue Za Zhi. 2014 Jan;43(1):15-9.
[Article in Chinese]

Abstract

Objective: To investigate methylation status of Wif-1 and β-catenin expression in colorectal serrated lesions.

Methods: Various colorectal lesions were collected including 52 cases of hyperplastic polyps, 41 cases of sessile serrated adenoma, 23 cases of traditional serrated adenoma, 24 cases of colorectal cancer and 24 cases of normal mucosa. All specimens were subject to immunohistochemical staining of β-catenin.SYBR Green PCR analysis of Wif-1 promoter methylation was performed in 29 cases of hyperplastic polyps, 29 cases of sessile serrated adenoma, 19 cases of traditional serrated adenoma, 14 cases of colorectal cancer and 16 cases of normal mucosa.

Results: Abnormal expression rates of β-catenin in normal mucosa, hyperplastic polyps, sessile serrated adenoma, traditional serrated adenoma and colorectal cancer were 12.5% (3/24), 59.6% (31/52), 63.4% (26/41), 73.9% (17/23) and 100.0% (24/24), respectively. The corresponding methylation rates of Wif-1 promoter were 2/16, 10/29 (34.5%), 16/29 (55.2%), 15/19 and 13/14 (P < 0.05), respectively. Abnormal β-catenin expression was positively correlated with Wif-1 promoter methylation in traditional serrated adenomas (r = 0.536, P < 0.05).

Conclusions: Abnormal β-catenin expression and methylation rate of Wif-1 promoter are significantly higher in colorectal serrated lesions. Methylation of Wif-1 promoter may be related to the abnormal expression of β-catenin through activation of Wnt/β-catenin signaling pathway, which may contribute to the development of colorectal serrated lesions.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics*
  • Adaptor Proteins, Signal Transducing / metabolism
  • Adenoma* / genetics
  • Adenoma* / metabolism
  • Adenoma* / pathology
  • Carcinoma / genetics
  • Carcinoma / metabolism
  • Carcinoma / pathology
  • Colorectal Neoplasms* / genetics
  • Colorectal Neoplasms* / metabolism
  • Colorectal Neoplasms* / pathology
  • DNA Methylation*
  • Humans
  • Hyperplasia
  • Immunohistochemistry
  • Intestinal Mucosa / metabolism
  • Intestinal Polyps* / pathology
  • Repressor Proteins / genetics*
  • Repressor Proteins / metabolism
  • Wnt Signaling Pathway
  • beta Catenin / metabolism*

Substances

  • Adaptor Proteins, Signal Transducing
  • CTNNB1 protein, human
  • Repressor Proteins
  • WIF1 protein, human
  • beta Catenin