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Differential expression of the eukaryotic release factor 3 (eRF3/GSPT1) according to gastric cancer histological types

机译:根据胃癌的组织学类型,真核生物释放因子3(eRF3 / GSPT1)的差异表达

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摘要

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 wasdetermined 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 revealedeRF3/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 intumorigenesis as a result of its non-translational roles, namely (dis)regulating the cell cycle, apoptosis, ortranscription.
机译:背景:现在有几条证据表明蛋白质合成和翻译因子参与细胞增殖和癌症发展的调控。目的:探讨真核生物释放因子3(eRF3)在胃癌中的基因表达模式。方法:从25例胃肿瘤活检组织和邻近的非肿瘤性粘膜中制备RNA。进行实时TaqMan逆转录聚合酶链反应(RT-PCR)以测量相对基因表达水平。从肿瘤和正常组织中分离DNA,并使用SYBR Green染料通过实时定量PCR测定基因剂量。结果:分析了胃癌的不同组织学类型,在25种肿瘤中有9种显示eRF3 / GSPT1过表达。此外,分析的12种肠型癌中有8种过表达该基因,而eRF3 / GSPT1在10种弥散型癌中仅一种过表达(Kruskal-Wallis检验; p = 0.05)。在eRF3 / GSPT1的倍性和转录本表达水平之间未发现相关性。 eRF3 / GSPT1的过表达与翻译速率增加无关,因为eRF3 / GSPT1的上调与eRF1水平升高无关。结论:eRF3 / GSPT1在肠型胃肿瘤中的过度表达可能导致特定致癌转录本的翻译效率提高。备选地,eRF3 / GSPT1可能由于其非翻译作用而参与肿瘤发生,即(失调)调节细胞周期,凋亡或转录。

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