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首页> 美国卫生研究院文献>Oncotarget >4EGI-1 induces apoptosis and enhances radiotherapy sensitivity in nasopharyngeal carcinoma cells via DR5 induction on 4E-BP1 dephosphorylation
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4EGI-1 induces apoptosis and enhances radiotherapy sensitivity in nasopharyngeal carcinoma cells via DR5 induction on 4E-BP1 dephosphorylation

机译：4EGI-1通过DR5诱导4E-BP1去磷酸化诱导鼻咽癌细胞凋亡并增强放射治疗敏感性

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The eIF4F complex regulated by a various group of eIF4E-binding proteins (4E-BPs) can initial the protein synthesis. Small molecule compound 4EGI-1, an inhibitor of the cap-dependent translation initiation through disturbing the interaction between eIF4E and eIF4G which are main elements of the eIF4E complex, has been reported to suppress cell proliferation by inducing apoptosis in many types of cancer. And death receptor 5 (DR5) is a major component in the extrinsic apoptotic pathway. However, the correlation among 4EGI-1, DR5 and 4E-BPs have not been discovered in NPC now. Therefore, we intend to find out the effect of 4EGI-1 on the apoptosis process of NPC and the relationship among 4EGI-1, DR5 and 4E-BPs. Our results revealed a significant down regulation of DR5 expression in NPC tissues, which inversely correlated with lymph node metastasis status and clinical stages. Depressed DR5 expression was an independent biomarker for poor prognosis in NPC, and elevated DR5 expression showed longer overall survival time in 174 NPC patients. Besides, 4EGI-1 induced apoptosis in NPC cells through the DR5-caspase-8 axis on 4E-BP1 and eIF4E dephosphorylation exerting positive influence on their anti-tumor activities. The induction of DR5 also sensitized NPC cells to radiotherapy, and the SER was 1.195. These results establish the death receptor pathway as a novel anticancer mechanism of eIF4E/eIF4G interaction inhibitor in NPC.
机译：由各种eIF4E结合蛋白（4E-BP）调控的eIF4F复合物可以启动蛋白质合成。据报道，小分子化合物4EGI-1是通过干扰eIF4E复合物的主要成分eIF4E和eIF4G之间的相互作用而引起的帽依赖性翻译起始的抑制剂，已通过诱导许多类型癌症的细胞凋亡来抑制细胞增殖。死亡受体5（DR5）是外在凋亡途径中的主要成分。但是，目前尚未在NPC中发现4EGI-1，DR5和4E-BP之间的相关性。因此，我们打算发现4EGI-1对NPC凋亡过程的影响以及4EGI-1，DR5和4E-BP之间的关系。我们的结果显示，NPC组织中DR5表达明显下调，这与淋巴结转移状况和临床阶段呈负相关。 DR5表达降低是NPC预后不良的独立生物标志物，DR5表达升高表明174名NPC患者的总生存时间更长。此外，4EGI-1通过4E-BP1上的DR5-caspase-8轴诱导NPC细胞凋亡，并通过eIF4E磷酸化对其抗肿瘤活性产生积极影响。 DR5的诱导也使NPC细胞对放射治疗敏感，SER为1.195。这些结果建立了死亡受体途径，作为NPC中eIF4E / eIF4G相互作用抑制剂的新型抗癌机制。

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