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Carcinogenesis Advance Access published online on June 29, 2005
Carcinogenesis, doi:10.1093/carcin/bgi168
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received May 12, 2005
Revised June 17, 2005
Accepted June 18, 2005

CANCER BIOLOGY

Polyglycine expansions in eRF3/GSPT1 are associated with gastric cancer susceptibility

M. Brito 1*, J. Malta-Vacas 1, B. Carmona 1, C. Aires 1, P. Costa 1, A. P. Martins 2, S. Ramos 2, A. R. Conde 3, and C. Monteiro 3

1 Escola Superior de Tecnologia da Saúde de Lisboa, Lisboa, Portugal
2 Serviço de Anatomia Patológica, Hospital de Santa Cruz, Lisboa, Portugal
3 Faculdade de Farmácia da Universidade de Lisboa, Lisboa, Portugal

* To whom correspondence should be addressed.
M. Brito, E-mail: miguel.brito{at}estesl.pt


  Abstract

Gastric cancer remains a major cause of death in the developed countries, and a large percentage is still genetically unexplained. Because of their major role in cell survival, mutations in translation factors and altered expression of these genes have been associated with cancer development. Apart from its role in translation termination, the eukaryotic translation release factor 3 (eRF3) is involved in several critical cellular processes, such as cell cycle regulation, cytoskeleton organization and apoptosis. The aim of this study was to evaluate eRF3/GSPT1 gene as a potential genetic susceptibility associated locus for gastric cancer, analysing a stable GGC expansion in exon 1 encoding a polyglycine tract in the amino-terminal domain of the protein. DNA was obtained from 139 patients with gastric cancer and from 100 individuals of a healthy control population. The GGC expansion was amplified by PCR and the number of repeats determined by genotyping in an automatic sequencer. There are five known alleles encoding from 8 to 12 glycines. The most common allele encodes 10 glycines. The 12-Gly allele was detected exclusively in the cancer patients (allelic frequency = 5%). Regardless of the genotype, patients with the 12-Gly allele had a 20-fold increased risk for gastric cancer. We also detected a single-base alteration in the gene (G1755C) although no correlation with cancer development has been found. Thus our results show that the GGC expansion may have a potential role in regulating eRF3/GSPT1 expression and/or changing the protein function that can lead to gastric cancer development.


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