Promoter hypermethylation and silencing of CHFR mitotic stress checkpoint gene in human gastric cancers

Hio Chung Kang, Il Jin Kim, Jae Hyun Park, Yong Shin, Hye Won Park, Ja Lok Ku, Han Kwang Yang, Kuhn Uk Lee, Kuk Jin Choe, Jae Gahb Park

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22 Scopus citations


CHFR is a recently identified mitotic stress checkpoint gene. CHFR is ubiquitously expressed in normal human tissues, whereas loss of CHFR expression has been observed in human tumors. Silencing of CHFR has been associated with aberrant promoter methylation and histone deacetylation in several cancer types. In this study, we investigated epigenetic CHFR inactivation in human gastric cancers by examining CHFR expression and methylation status in gastric cancer cell lines with RT-PCR analysis, bisulfite PCR and sequencing. A series of primary gastric tumors were also analyzed for CHFR methylation. Eight of 12 (66.7%) gastric cancer cell lines and 19/43 (44.2%) primary gastric tumors showed CHFR methylation. In addition, CpG methylation status correlated well with CHFR expression in the human gastric cancer cell lines, in which treatment with 5-aza-dC resulted in de novo or enhanced expression of CHFR. Combination treatment of 5-aza-dC with trichostatin A showed a synergistic effect on CHFR expression in some cases. Our results indicate that aberrant promoter methylation of the CHFR gene was observed in a significant proportion of human gastric cancers and was responsible for the inactivation of the CHFR gene in gastric cancers.

Original languageEnglish
Pages (from-to)129-133
Number of pages5
JournalOncology Reports
Issue number1
StatePublished - 1 Jul 2004


  • CHFR
  • Gastric cancer
  • Promoter methylation
  • Silencing

Cite this

Kang, H. C., Kim, I. J., Park, J. H., Shin, Y., Park, H. W., Ku, J. L., Yang, H. K., Lee, K. U., Choe, K. J., & Park, J. G. (2004). Promoter hypermethylation and silencing of CHFR mitotic stress checkpoint gene in human gastric cancers. Oncology Reports, 12(1), 129-133.