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Frequent loss of imprinting of IGF2 and MEST in lung adenocarcinoma
Author(s) -
Kohda Masakazu,
Hoshiya Hidetoshi,
Katoh Motonobu,
Tanaka Isao,
Masuda Ryo,
Takemura Tamiko,
Fujiwara Mutsunori,
Oshimura Mitsuo
Publication year - 2001
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.1053
Subject(s) - genomic imprinting , biology , imprinting (psychology) , loss of heterozygosity , carcinogenesis , genetics , gene , gene silencing , allele , gene expression , regulation of gene expression , cancer research , dna methylation
Genomic imprinting is a parental origin–specific chromosomal modification that causes differential expression of maternal and paternal alleles of a gene. Accumulating evidence suggests that deregulation of imprinted genes, including loss of imprinting (LOI), plays a role in oncogenesis. In the present study, we investigated allelic expression of six imprinted genes in human lung adenocarcinomas as well as in matched normal lung tissue. Informative cases showing heterozygosity for the gene of interest were selected from 35 patients. LOI of the insulin‐like growth factor 2 gene ( IGF2 ) and mesoderm‐specific transcript ( MEST , also known as paternally expressed gene 1) was noted in 47% (seven of 15) and 85% (11 of 13) of informative cases, respectively. Monoallelic expression was maintained in all the matched normal tissues examined. LOI of IGF2 was seen more frequently in moderately to poorly differentiated adenocarcinomas. In contrast, H19 , small nuclear ribonucleoprotein–associated polypeptide N gene ( SNRPN ), necdin gene ( NDN ), and long QT intronic transcript 1 ( LIT1 ) exhibited consistent monoallelic expression in all the informative samples. These findings indicated that independent deregulation took place in imprinted genes and suggested that aberrant imprinting of IGF2 and MEST was involved in the development of lung adenocarcinoma. © 2001 Wiley‐Liss, Inc.