eEF2K与肿瘤

Eukaryotic elongation factor 2 kinase and cancer

真核延伸因子激酶-2(eukaryotic elongation factor 2 kinase,e EF2K)属于特殊的蛋白激酶——α-激酶小家族,并且是该家族中唯一的Ca^(2+)/Ca M依赖性蛋白激酶。e EF2K催化真核延伸因子-2(eukaryotic elongation factor 2,e EF2)的Thr56位点发生磷酸化并导致其失活,从而抑制肽链延伸过程。除了受Ca^(2+)/Ca M调控,e EF2K还受到营养、能量相关信号分子如AMPK、m TORC1等的调控。近年来研究表明,e EF2K在多种肿瘤组织及细胞中高表达,并参与肿瘤生长、细胞周期、自噬、凋亡、血管新生、侵袭转移等过程的调控。因此e EF2K可能是潜在的肿瘤治疗靶点。本文就e EF2K的结构、调控,以及与肿瘤的恶性进程、治疗及预后等关系进行综述。

Eukaryotic elongation factor 2 kinase（e EF2K） belongs to the small family of atypical kinase-α-kinase, and is the only Ca^（2＋）/Calmodulin（Ca M）-dependent protein kinase of the family. e EF2 K catalyzes the Thr56 phosphorylation site of eukaryotic elongation factor 2（e EF2） and subsequently inactivates e EF2, thereby negatively modulates m RNA translation. In addition to activated by Ca^（2＋）/Ca M, e EF2 K is also modulated by nutrition and energy related signaling molecules such as AMPK, m TORC1 etc. Recently it has been found that e EF2 K protein has high expression in several tumor tissues and cells. Meanwhile it has participated in modulating growth, cell cycle, autophagy, apoptosis, angiogenesis, invation and metastasis of cancer cells. Therefore e EF2 K emerges as a potential target for future cancer therapy. The knowledge about the structure and regulation of e EF2 K, and the relationship between e EF2 K and tumor progression, therapy, prognosis are summarized in this article.