The role of eukaryotic translation initiation factor 6 in tumors.
The role of eukaryotic translation initiation factor 6 in tumors.
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真核翻译起始因子6在肿瘤中的作用
DOI：
10.3892/ol.2017.6161
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发表时间：
2017-07
期刊：
影响因子：
2.9
通讯作者：
Liu XY
中科院分区：
文献类型：
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作者：
Zhu W;Li GX;Chen HL;Liu XY
真核翻译起始因子6（eIF 6）影响60 S核糖体亚基的成熟。在酵母和哺乳动物细胞中发现，eIF 6主要位于哺乳动物细胞的细胞质中。新出现的证据表明，eIF 6的表达失调在几种类型的人类癌症中是重要的，包括头颈癌、结直肠癌、非小细胞肺癌和卵巢浆液性腺癌。然而，eIF 6在肿瘤形成和发展过程中发挥作用的分子机制仍然难以捉摸。本文综述了eIF 6在人类肿瘤发生和肿瘤细胞系中的作用机制和功能，沿着这种新型翻译起始因子可能参与的信号转导途径。致癌Ras通过Hairless依赖性机制的重组结合蛋白抑制子激活Notch-1并促进eIF 6的转录。此外，eIF 6的过表达导致Wnt/β-连环蛋白信号通路的异常激活。类似地，过度表达的eIF 6调节其下游调节物，细胞分裂控制蛋白42，这反过来又影响肿瘤发生。最后，eIF 6作为诊断癌症的生物标志物的潜力也在本综述中进行了讨论。
Eukaryotic translation initiation factor 6 (eIF6) affects the maturation of 60S ribosomal subunits. Found in yeast and mammalian cells, eIF6 is primarily located in the cytoplasm of mammalian cells. Emerging evidence has demonstrated that the dysregulated expression of eIF6 is important in several types of human cancer, including head and neck carcinoma, colorectal cancer, non-small cell lung cancer and ovarian serous adenocarcinoma. However, the molecular mechanisms by which eIF6 functions during tumor formation and progression remain elusive. The present review focuses on recent progress in terms of the mechanisms and functions of eIF6 in human tumorigenesis or cancer cell lines, along with the signal transduction pathways in which this novel translation initiation factor may participate. Oncogenic Ras activates Notch-1 and promotes transcription of eIF6 via a recombining binding protein suppressor of Hairless-dependent mechanism. In addition, overexpression of eIF6 results in aberrant activation of the Wnt/β-catenin signaling pathway. Similarly, overexpressed eIF6 regulates its downstream modulator, cell division control protein 42, which in turn affects oncogenesis. Finally, the potential of eIF6 as a biomarker for diagnosis of cancer is also discussed in the present review.
DOI：
10.5114/aoms.2013.36753
发表时间：
2014-02-24
期刊：
Archives of medical science : AMS
影响因子：
--
作者：
Gottwald L;Danilewicz M;Fendler W;Suzin J;Spych M;Piekarski J;Tylinski W;Chalubinska J;Topczewska-Tylinska K;Cialkowska-Rysz A
通讯作者：
Cialkowska-Rysz A