EEF1E1 promotes glioma proliferation by regulating cell cycle through PTEN/AKT signaling pathway
EEF1E1 promotes glioma proliferation by regulating cell cycle through PTEN/AKT signaling pathway
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EEF 1 E1通过PTEN/AKT信号通路调控细胞周期促进胶质瘤增殖
DOI：
10.1002/mc.23611
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发表时间：
2023-08-17
影响因子：
4.6
通讯作者：
Pan，Yawen
中科院分区：
文献类型：
--
作者：
Wang，Hongyu;Han，Ruiqin;Pan，Yawen
细胞周期是细胞增殖的关键调控因子，可受磷酸酶和紧张素同源物(PTEN)/AKT信号通路对细胞周期蛋白相关蛋白的调控。在我们的研究中，我们发现了EEF1E1在这一过程中的关键作用，因为它似乎下调了PTEN的表达。此外，我们的研究结果证实，EEF1E1通过抑制PTEN/AKT通路调节下游细胞周期相关蛋白。细胞周期分析结果显示，EEF1E1下调抑制胶质瘤细胞在G1期和S期的进展。细胞计数试剂盒- 8、集落形成和乙基- 2 ' -脱氧尿苷等一系列实验证实，EEF1E1下调可显著抑制胶质瘤的增殖。我们通过动物实验和脑切片共培养实验进一步验证了这一现象。综合研究表明，EEF1E1敲低可通过PTEN/AKT信号通路调控细胞周期，有效抑制胶质瘤细胞增殖。因此，EEF1E1成为胶质瘤治疗的潜在治疗靶点，具有重要的临床意义。
The cell cycle, a pivotal regulator of cell proliferation, can be significantly influenced by the phosphatase and tensin homolog (PTEN)/AKT signaling pathway's modulation of cyclin‐related proteins. In our study, we discovered the crucial role of EEF1E1 in this process, as it appears to downregulate PTEN expression. Furthermore, our findings affirmed that EEF1E1 modulates downstream cell cycle‐related proteins by suppressing the PTEN/AKT pathway. Cell cycle assay results revealed that EEF1E1 downregulation stunted the advancement of glioma cells in both the G1 and S phases. A suite of assays—Cell Counting Kit‐8, colony formation, and ethyl‐2’‐deoxyuridine—substantiated that the EEF1E1 downregulation markedly curtailed glioma proliferation. We further validated this phenomenon through animal studies and coculture experiments on brain slices. Our comprehensive investigation indicates that EEF1E1 knockdown can effectively inhibit the glioma cell proliferation by regulating the cell cycle via the PTEN/AKT signaling pathway. Consequently, EEF1E1 emerges as a potential therapeutic target for glioma treatment, signifying critical clinical implications.