Scholarlink

<p>Glioma is a malignant central nervous system tumor that poses a threat to patient survival. Eukaryotic translation initiation factor 2 subunit alpha (EIF2S1) is closely associated with the progression of multiple human cancers. This study aimed to investigate the effects of EIF2S1 on glioma cells and the underlying molecular mechanisms. We analyzed EIF2S1 expression in glioma tissues and cell lines. Small interfering RNA (siRNA) targeting EIF2S1 was constructed and transfected into glioma cell lines to silence EIF2S1 expression. We then evaluated cell proliferation, apoptosis, and metastatic capacity. Western blotting (WB) was used to determine the effect of EIF2S1 knockdown on the phosphorylation levels of PI3K and AKT. Finally, glioma cells were co-treated with the PI3K activator 740 Y-P to verify whether the PI3K/AKT pathway mediates the function of EIF2S1 in glioma cells. EIF2S1 was significantly up-regulated in glioma. Knockdown of EIF2S1 markedly inhibited glioma cell proliferation, promoted apoptosis, and suppressed metastatic potential. Western blot analysis indicated that EIF2S1 silencing significantly reduced the phosphorylation levels of PI3K and AKT. Moreover, 740 Y-P significantly reversed the inhibitory effect of si-EIF2S1 on glioma cells. Our <i>in vitro</i> findings suggeste that EIF2S1 contributes the malignant progression of glioma cells by regulating the PI3K/AKT pathway, providing a theoretical basis for future exploring EIF2S1 as a potentical therapeutic target for glioma.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Inhibition of EIF2S1 expression regulates the PI3K/AKT pathway to mediate apoptosis in glioma cells: an in vitro study

  • 期刊论文

  • 发表日期：

    2026年5月29日

查看全文
  • Gang Li,
  • Min Wang,
  • Na Wei,
  • Zheng Qiu

摘要

Glioma is a malignant central nervous system tumor that poses a threat to patient survival. Eukaryotic translation initiation factor 2 subunit alpha (EIF2S1) is closely associated with the progression of multiple human cancers. This study aimed to investigate the effects of EIF2S1 on glioma cells and the underlying molecular mechanisms. We analyzed EIF2S1 expression in glioma tissues and cell lines. Small interfering RNA (siRNA) targeting EIF2S1 was constructed and transfected into glioma cell lines to silence EIF2S1 expression. We then evaluated cell proliferation, apoptosis, and metastatic capacity. Western blotting (WB) was used to determine the effect of EIF2S1 knockdown on the phosphorylation levels of PI3K and AKT. Finally, glioma cells were co-treated with the PI3K activator 740 Y-P to verify whether the PI3K/AKT pathway mediates the function of EIF2S1 in glioma cells. EIF2S1 was significantly up-regulated in glioma. Knockdown of EIF2S1 markedly inhibited glioma cell proliferation, promoted apoptosis, and suppressed metastatic potential. Western blot analysis indicated that EIF2S1 silencing significantly reduced the phosphorylation levels of PI3K and AKT. Moreover, 740 Y-P significantly reversed the inhibitory effect of si-EIF2S1 on glioma cells. Our in vitro findings suggeste that EIF2S1 contributes the malignant progression of glioma cells by regulating the PI3K/AKT pathway, providing a theoretical basis for future exploring EIF2S1 as a potentical therapeutic target for glioma.