Biallelic expression of the H19 and IGF2 genes in hepatocellular carcinoma

Cited 62 time in scopus
Metadata Downloads
Title
Biallelic expression of the H19 and IGF2 genes in hepatocellular carcinoma
Author(s)
Kyoung-Sook Kim; Young Ik Lee
Bibliographic Citation
Cancer Letters, vol. 119, pp. 143-148
Publication Year
1997
Abstract
The imprinted genes, H19 and insulin-like growth factor II (IGF2), have been demonstrated to be necessary for embryonal development in humans. Both genes are reciprocally imprinted, with expression of the maternal H19 and paternal IGF2 alleles, and are normally characterized by monoallelic expression. Recently, loss of imprinting of these genes producing biallelic expression has been observed in childhood tumors including Wilms' tumors (WT), embryonal rhabdomyosarcoma, and adulthood tumors such as lung cancer. To test the existence of loss of imprinting in hepatocellular carcinoma (HCC), we analyzed the status of imprinting of H19 and IGF2 genes in three independent tumors, three HCC and one hepatoblastoma cell lines using AluI and ApaI polymorphisms of these genes, respectively. In contrast to the previous report, all the cases except one tumor and one HCC cell line showed biallelic expression of both H19 and IGF2 genes. Unlike WT, loss of imprinting (LOI) of IGF2 in HCC was not linked to down-regulation of H19 expression, but rather associated with coexpression for H19 and IGF2. Thus, H19 and IGF2 expression can be uncoupled in tumors with LOI. The frequent biallelic expression of H19 and IGF2 in hepatocellular carcinoma might play a causal role in the epigenetic mechanism involved in tumor development and/or process.
Keyword
Insulin-like growth factor II (IGF2)H19 geneLoss of imprinting (LOI)Hepatocellular carcinoma (HCC)Hep3B
ISSN
0304-3835
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/S0304-3835(97)00264-4
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.