Graff Jeremy R, Konicek Bruce W, Carter Julia H, Marcusson Eric G
Cancer Growth and Translational Genetics, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana 46285, USA.
Cancer Res. 2008 Feb 1;68(3):631-4. doi: 10.1158/0008-5472.CAN-07-5635.
The eukaryotic translation initiation factor 4E (eIF4E) is frequently overexpressed in human cancers in relation to disease progression and drives cellular transformation, tumorigenesis, and metastatic progression in experimental models. Enhanced eIF4E function results from eIF4E overexpression and/or activation of the ras and phosphatidylinositol 3-kinase/AKT pathways and selectively increases the translation of key mRNAs involved in tumor growth, angiogenesis, and cell survival. Consequently, by simultaneously and selectively reducing the expression of numerous potent growth and survival factors critical for malignancy, targeting eIF4E for inhibition may provide an attractive therapy for many different tumor types. Recent work has now shown the plausibility of therapeutically targeting eIF4E and has resulted in the advance of the first eIF4E-specific therapy to clinical trials. These studies illustrate the increased susceptibility of tumor tissues to eIF4E inhibition and support the notion that the enhanced eIF4E function common to many tumor types may represent an Achilles' heel for cancer.
真核生物翻译起始因子4E(eIF4E)在人类癌症中常与疾病进展相关而过度表达,并在实验模型中驱动细胞转化、肿瘤发生和转移进展。eIF4E功能增强源于eIF4E的过度表达和/或ras及磷脂酰肌醇3激酶/AKT信号通路的激活,并选择性增加参与肿瘤生长、血管生成和细胞存活的关键mRNA的翻译。因此,通过同时并选择性地降低对恶性肿瘤至关重要的多种强效生长和存活因子的表达,靶向抑制eIF4E可能为许多不同类型的肿瘤提供一种有吸引力的治疗方法。最近的研究表明了治疗性靶向eIF4E的可行性,并促使首个eIF4E特异性疗法进入临床试验阶段。这些研究说明了肿瘤组织对eIF4E抑制的敏感性增加,并支持了许多肿瘤类型中常见的eIF4E功能增强可能是癌症致命弱点的观点。