真核延长因子Ⅱ激酶在肿瘤细胞中的作用

The Role of Eukaryotic Elongation Factor Ⅱ Kinase in Tumor Cells

真核延长因子Ⅱ激酶(eE F2K)是一个在钙调蛋白通路中结构和功能上比较独特的蛋白激酶。eE F2K可以在蛋白质合成、细胞周期及在肿瘤细胞中诱导自噬和凋亡,且在蛋白质延伸过程中起一个关键作用。其下游基因真核延长因子Ⅱ(eE F2)属于GTP家族成员是蛋白质合成所必需的,eE F2K磷酸化eE F2,从而抑制eE F2的活性阻止蛋白质的正常合成。近年来,在脑胶质瘤、乳腺癌等多种肿瘤中报道eE F2K表达上调,促进肿瘤的发生、发展。因此,进一步探讨eE F2K在肿瘤细胞中的潜在分子机制,将有望成为肿瘤治疗中新的生物指标和药物靶点。

Eukaryotic elongation factor 2 kinase （eEF2K） is a structurally and functionally unique pro- tein kinase in the calmodulin-mediated signaling pathway, eEF2K regulates numerous processes, such as protein synthesis, cell cycle andinduction of autophagy and apoptosis in cancer cells, and plays a key role in protein synthesis. Eukaryotic elongation factor 2 （eEF2） is a member of the GTP-binding translation elongation factor family that is essential for protein synthesis, eEF2K phosphorylates eEF2, thereby inhibits eEF2 function and inhibits protein synthesis. In recent years ,there are reports about eEF2K upregulation in glioma, breast cancer and other cancers, promoting tumor progression. Therefore, further exploration of the molecular mechanisms underlying eEF2K in tumor cells is being done, expecting it to become a novel biomarker and therapeutic target for tumor treatment.