Publication: Hyper-methylation of RIZ1 tumor suppressor gene is involved in the early tumorigenesis of hepatocellular carcinoma
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Date
2008
Authors
Piao, G-H. ; Piao, W-H. ; He, Y. ; Zhang, H. ; Wang, G-Q. ; Piao, Z.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The retinoblastoma protein-interacting zinc
finger gene RIZ1 is a putative tumor suppressor gene,
and the inactivation of the RIZ1 is frequently found in
tumors through a loss of mRNA expression. In order to
understand the role of RIZ1 inactivation in the
tumorigenesis of hepatocellular carcinoma (HCC), we
detected the RIZ1 promoter methylation status in 39
HCCs using a methylation specific PCR (MSP) method,
and carried out LOH study with marker P704. We also
assessed the associations between the methylation status
and clinicopathological parameters, tumor size, tumor
differentiation, and fractional allelic loss (FAL). The
results showed that the RIZ1 promoter methylated both
in advanced tumors (>3 cm), (18/31, 58.0%) and in early
tumors (<3 cm), (4/8, 50.0%). There were 54.6% (12/22)
tumors with hyper-methylation in the low FAL group
and 45.5% (10/22) in the high FAL group. Moreover, the
DNA methylation of the RIZ1 promoter was found not
only in the poorly differentiated tumors (12/22, 54.6%),
but also in the well differentiated tumors (10/22, 45.5%).
Among the 22 HCCs (22/39, 56.4%) that showed hypermethylation
at the RIZ1 promoter region, 3 cases showed
biallelic methylation. Interestingly, one case showed
hyper-methylation on one allele and a loss of
heterozygosity (LOH) on the other allele. In other words,
4 HCCs showed the biallelic inactivation of the RIZ1. These results suggest that the inactivation of the RIZ1 by
DNA methylation at its promoter region is involved in
the tumorigenesis of HCC, particularly in the early stage
of disease.
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