EEF1D 通过 EMT 和 PI3K/Akt 通路促进胶质瘤的增殖、迁移和侵袭。
EEF1D Promotes Glioma Proliferation, Migration, and Invasion through EMT and PI3K/Akt Pathway.
机构信息
Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515 Guangdong, China.
Department of Neurosurgery, The Second Affiliated Hospital of the Chinese University of Hong Kong (Shenzhen), Shenzhen, 518116 Guangdong, China.
出版信息
Biomed Res Int. 2020 Sep 24;2020:7804706. doi: 10.1155/2020/7804706. eCollection 2020.
Eukaryotic translation elongation factor 1 (EEF1D), a subunit of the elongation factor 1 complex of proteins, mediates the elongation process of protein synthesis. Besides this canonical role, EEF1D was found overexpressed in many tumors, like hepatocarcinomas and medulloblastomas. In the present study, we demonstrated for the first time that EEF1D may interact with other putative proteins to regulate cell proliferation, migration, and invasion through PI3K/Akt and EMT pathways in glioma. Furthermore, knockdown of EEF1D could reduce cell proliferation and impaired epithelial-mesenchymal transition (EMT) phenotypes, including cell invasion. Taken together, these results indicate that EEF1D and its partner proteins might play a critical role in glioma and serve as a potential therapeutic target of glioma.
真核翻译延伸因子 1（EEF1D）是蛋白质延伸因子 1 复合物的一个亚基，介导蛋白质合成的延伸过程。除了这个典型的作用，EEF1D 在许多肿瘤中被发现过度表达，如肝癌和髓母细胞瘤。在本研究中，我们首次证明 EEF1D 可能与其他假定的蛋白质相互作用，通过 PI3K/Akt 和 EMT 途径调节胶质瘤中的细胞增殖、迁移和侵袭。此外，EEF1D 的敲低可降低细胞增殖并损害上皮-间充质转化（EMT）表型，包括细胞侵袭。总之，这些结果表明 EEF1D 及其伴侣蛋白可能在神经胶质瘤中发挥关键作用，并可能成为神经胶质瘤的潜在治疗靶点。
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