Differential expression of the eukaryotic release factor 3 (eRF3/GSPT1) accordi...

• Author(s): Malta-Vacas, Joana ; Aires, C. ; Costa, P. ; Conde, A. R. ; Ramos, S. ; Martins, A. P. ; Monteiro, C. ; Brito, Miguel
• Date: 2005
• Persistent ID: http://hdl.handle.net/10400.21/2982
• Origin: Repositório Científico do Instituto Politécnico de Lisboa
• Subject(s): DNA, Neoplasm/genetics; Gene dosage; Neoplasm proteins/genetics; Neoplasm proteins/metabolism; Peptide termination factors/genetics; Peptide termination factors/metabolism; RNA, Neoplasm/genetics; Reverse Transcriptase Polymerase Chain Reaction/methods; Stomach neoplasms; Up-regulation
• Document Type: Article
• Language: English

Description

Background: There are now several lines of evidence to suggest that protein synthesis and translation factors are involved in the regulation of cell proliferation and cancer development. Aims: To investigate gene expression patterns of eukaryotic releasing factor 3 (eRF3) in gastric cancer. Methods: RNA was prepared from 25 gastric tumour biopsies and adjacent non-neoplastic mucosa. Real time TaqMan reverse transcription polymerase chain reaction (RT-PCR) was performed to measure the relative gene expression levels. DNA was isolated from tumour and normal tissues and gene dosage was determined by a quantitative real time PCR using SYBR Green dye. Results: Different histological types of gastric tumours were analysed and nine of the 25 tumours revealed eRF3/GSPT1 overexpression; moreover, eight of the 12 intestinal type carcinomas analysed overexpressed the gene, whereas eRF3/GSPT1 was overexpressed in only one of the 10 diffuse type carcinomas (Kruskal-Wallis Test; p , 0.05). No correlation was found between ploidy and transcript expression levels of eRF3/GSPT1. Overexpression of eRF3/GSPT1 was not associated with increased translation rates because the upregulation of eRF3/GSPT1 did not correlate with increased eRF1 levels. Conclusions: Overexpression of eRF3/GSPT1 in intestinal type gastric tumours may lead to an increase in the translation efficiency of specific oncogenic transcripts. Alternatively, eRF3/GSPT1 may be involved in tumorigenesis as a result of its non-translational roles, namely (dis)regulating the cell cycle, apoptosis, or transcription.