Protein synthesis via translation is a central process involving several essential proteins called translation factors. Although traditionally described as cellular “housekeepers,” multiple studies have now supported that protein initiation and elongation factors regulate cell growth, apoptosis, and tumorigenesis. One such translation factor is eukaryotic elongation factor 1 alpha 2 (EEF1A2), a member of the eukaryotic elongation factor family, which has a canonical role in the delivery of aminoacyl-tRNA to the A-site of the ribosome in a guanosine 5′-triphosphate (GTP)-dependent manner. EEF1A2 differs from its closely related isoform, EEF1A1, in tissue distribution. While EEF1A1 is present ubiquitously, EEF1A2 replaces it in specialized tissues. The reason why certain specialized tissues need to essentially switch EEF1A1 expression altogether with EEF1A2 remains to be answered. Abnormal “switch on” of the EEF1A2 gene in normal tissues is witnessed and is seen as a cause of oncogenic transformation in a wide variety of solid tumors. This review presents the journey of finding increased expression of EEF1A2 in multiple cancers, establishing molecular mechanism, and exploring it as a target for cancer therapy. More precisely, we have compiled studies in seven types of cancers that have reported EEF1A2 overexpression. We have discussed the effect of aberrant EEF1A2 expression on the oncogenic properties of cells, signaling pathways, and interacting partners of EEF1A2. More importantly, in the last part, we have discussed the unique potential of EEF1A2 as a therapeutic target. This review article gives an up-to-date account of EEF1A2 as an oncogene and can draw the attention of the scientific community, attracting more research.

中文翻译：

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EEF1A2表达的致癌激活：从假定的致癌基因到确定的致癌基因的旅程

通过翻译合成蛋白质是一个核心过程，涉及几种称为翻译因子的必需蛋白质。尽管传统上被描述为细胞“管家”，但多项研究现在支持蛋白质起始和延伸因子调节细胞生长、凋亡和肿瘤发生。此类翻译因子之一是真核延伸因子 1 α 2 (EEF1A2)，它是真核延伸因子家族的一员，在将氨酰基-tRNA 递送至鸟苷 5'- 核糖体 A 位点方面发挥着重要作用。三磷酸（GTP）依赖性方式。EEF1A2 与其密切相关的异构体 EEF1A1 在组织分布上有所不同。虽然 EEF1A1 无处不在，但 EEF1A2 在特殊组织中取代了它。为什么某些特殊组织需要将 EEF1A1 表达与 EEF1A2 一起本质上转换的原因仍有待解答。正常组织中 EEF1A2 基因的异常“开启”已被证实，并且被视为多种实体瘤致癌转化的原因。这篇综述介绍了在多种癌症中发现 EEF1A2 表达增加、建立分子机制并探索其作为癌症治疗靶点的历程。更准确地说，我们整理了七种报告 EEF1A2 过度表达的癌症的研究。我们讨论了异常 EEF1A2 表达对细胞致癌特性、信号通路和 EEF1A2 相互作用伙伴的影响。更重要的是，在最后一部分中，我们讨论了 EEF1A2 作为治疗靶点的独特潜力。这篇综述文章提供了 EEF1A2 作为癌基因的最新描述，可以引起科学界的关注，吸引更多的研究。