APLASIA RAS HOMOLOGOUS MEMBER I GENE
AND DEVELOPMENT OF GLIAL TUMORS
Yakut S1, Tuncer MR2,* Berker M3, Goksu E2, Gurer I4, Ozes ON1, Luleci G1, Karauzum SB1
*Corresponding Author: Sibel Berker Karauzum, Department of Medical Biology and Genetics, Faculty
of Medicine, Akdeniz University Antalya, Turkey; Tel.: +90 242 2496971; Fax: +90 242 2274482; E-mail:
sibelkarauzum@akdeniz.edu.tr
page: 37
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Abstract
The ARHI (aplasia Ras homologue member I,
also known as DIRAS3) gene shows 60.0% sequence
homology to the Ras proto-oncogene and was the first
mater-nally-imprinted tumor suppressor gene identified
in the Ras family. It is constitutively expressed
from the paternal allele in normal breast, ovary, heart,
liver, pancreas, thyroid and brain tissues, and is lost or
markedly down-regulated primarily in breast, ovarian,
pancreas and thyroid tumor tissues. We have investigated
the expression, LOH (loss of heterozygosity) and
methylation status of this gene in glial tumors and peripheral
blood samples of 21 patients, and in seven normal
brain tissue samples. Gene expression by real time
reverse transcriptase polymerase chain reaction (RTPCR)
was found to be increased in 14 and decreased in
seven of the 21 tumors. The LOH was detected by fragment
analysis, using five labeled polymorphic markers
specific for the 1p31 region, in two of the tumors.
Methylation status of the CpG island I, II and III was
evaluated using COBRA (combined bisulfite restriction
analysis) and RFLP (restriction fragment length
polymorphism) in 21 tumors and also a hypermethylated
healthy volunteer as a positive control, revealed
that only two tumors had hypermethylation in CpG
island I (of which one also had LOH). These results
suggest that LOH and hypermethylation may be one
mechanism of silencing the ARHI gene expression and
development of glial tumor development.
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