The fragile histidine triad (
FHIT) gene is a tumor-associated gene, and aberrant
FHIT gene and protein expression have been described in many types of human tumors. Furthermore, it has been reported that
FHIT gene inactivation is induced by hypermethylation of 5' CpG islands in the gene or by genomic deletion around the open reading frame (ORF). In this study, we explored the aberrations in the canine
FHIT gene and Fhit protein expression and assessed the methylation status and genomic deletions by using 5 canine lymphoma cell lines. We found that the decrease in the expression of the Fhit protein in canine lymphoma cell lines was similar to that in human tumors. The expression of the wild-type
FHIT transcript was reduced in all 5 cell lines. However, we could not confirm the involvement of aberrant methylation events in the 5' CpG islands of the canine
FHIT gene. We were able to identify homozygous or heterozygous deletions in the canine
FHIT genes in all 5 cell lines. Moreover, a widespread genomic deletion of the
FHIT gene, which included the ORF region, was detected in 1 cell line. In the present study, we detected aberrations in the
FHIT gene and Fhit protein expression in all 5 canine lymphoma cell lines, and this phenomenon might be an important factor in promoting canine lymphoma.
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