[The role of hypermethylation in promoter region of ubiquitin carboxyl-terminal hydrolase L1 in human esophageal cancer]

Zhonghua Nei Ke Za Zhi. 2012 May;51(5):390-3.
[Article in Chinese]

Abstract

Objective: To study the association of ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) promoter region methylation with human esophageal cancer.

Methods: Promoter region methylation of UCHL1 was detected by methylation specific PCR (MSP) in esophageal cancer cell lines and tissue samples. The expression of UCHL1 was detected by semi-quantitative RT-PCR and Western blot in esophageal cancer cell lines. 5-Aza-2'-deoxycytidine (5-Aza) was applied to reactivate methylated cell lines.

Results: Complete methylation of UCHL1 promoter region was detected in 8 cell lines (KYSE30, KYSE150, KYSE140, KYSE450, KYSE510, TE3, TE7, TE10). Loss of UCHL1 expression was found in 7 cell lines (KYSE30, KYSE150, KYSE140, KYSE450, KYSE510, TE3, TE7). Reduced expression was found in TE10 cell line. Promoter region hypermethylation was correlated with UCHL1 expression in esophageal cancer cell lines. Re-expression of UCHL1 was induced by 5-Aza treatment in KYSE150 and TE3 cell lines. UCHL1 was frequently methylated in human primary esophageal cancer (74.51%, 38/51), while no methylation was detected in normal esophageal mucosa(0/10). No association was found between promoter region methylation and age, gender, tumor location, tumor stage or lymph node metastasis.

Conclusions: UCHL1 is silenced by promoter region hypermethylation in human esophageal cancer. Methylation of UCHL1 is frequently happened to primary esophageal cancer and may play an important role in the tumorigenesis.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Cell Line, Tumor
  • DNA Methylation*
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / metabolism*
  • Esophageal Neoplasms / pathology*
  • Female
  • Humans
  • Male
  • Middle Aged
  • Promoter Regions, Genetic*
  • RNA, Messenger / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Ubiquitin Thiolesterase / genetics
  • Ubiquitin Thiolesterase / metabolism*

Substances

  • RNA, Messenger
  • Ubiquitin Thiolesterase