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Carcinogenesis, Vol. 23, No. 10, 1695-1700, October 2002
© 2002 Oxford University Press

CARCINOGENESIS

Chfr expression is downregulated by CpG island hypermethylation in esophageal cancer

Yasuyuki Shibata*, Nobuhiro Haruki*, Yoshiyuki Kuwabara, Hideyuki Ishiguro, Noriyuki Shinoda, Atsushi Sato, Masahiro Kimura, Hiroshi Koyama, Tatsuya Toyama, Tadashi Nishiwaki, Junzo Kudo, Yukio Terashita, Shigeru Konishi, Hironori Sugiura and Yoshitaka Fujii1

Department of Surgery II, Nagoya City University Medical School, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan

Cell cycle progression is monitored by checkpoint mechanisms to ensure the integrity of the genome and the fidelity of sister chromatid separation. Failure of such checkpoint functions results in genomic instability, a condition that predisposes cells to neoplastic transformation and tumor progression. Recently, Scolnick and Halazonetis defined a new mitotic checkpoint that acts at prophase and delays chromosome condensation in response to mitotic stress, and identified a gene, named checkpoint with FHA and ring finger (Chfr), that seems to be required for delaying prophase in human cells. In the present study, we examined human Chfr mRNA expression in 15 human esophageal cancer cell lines and 43 primary esophageal cancers to investigate the potential involvement of Chfr in the pathogenesis of esophageal cancers. We report here that a significant proportion of human esophageal cancer has loss of expression of Chfr gene. Furthermore, we found aberrant hypermethylation of the promoter region of this checkpoint gene in four of 15 (26.7%) esophageal cancer cell lines and in seven of 43 (16.3%) primary cancers.


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