Scholarlink

<p>The progression of oral squamous cell carcinoma (OSCC), a frequent cancer of the mouth, has been associated with EIF2AK2 dysregulation, but its precise mechanisms are yet to be clarified. In this study, we investigated the expression of EIF2AK2 in OSCC tissues and cell lines using publicly available databases and Western blotting. EIF2AK2 was silenced using small interfering RNA (siRNA), and its functional impact on OSCC malignant characteristics was determined using several in vitro experiments. Additionally, we determined EIF2AK2’s impact on autophagy levels and the activity of mechanistic pathways. Our results demonstrate that EIF2AK2 is markedly overexpressed in OSCC tissues and cell lines, and its knockdown significantly affects OSCC malignant characteristics, such as proliferation, migration, and invasion. Furthermore, EIF2AK2 knockdown increased E-cadherin levels while reducing those of N-cadherin and Vimentin, supporting EMT suppression. It also led to reduced autophagy based on decreased LC3-II and Beclin-1 and increased p62 expressions. Moreover, inhibition of EIF2AK2 led to the downregulation of the JAK2/STAT3 axis. Collectively, these findings support EIF2AK2 as an oncogene in OSCC progression by activating autophagy through the JAK2/STAT3 pathway.</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

EIF2AK2 activates autophagy via JAK2/STAT3 pathway to promote oral squamous cell carcinoma malignancy

  • 期刊论文

  • 发表日期：

    2026年1月7日

查看全文
  • Xiaonan Zhang,
  • Xiangling Liao,
  • Zhen Du

摘要

The progression of oral squamous cell carcinoma (OSCC), a frequent cancer of the mouth, has been associated with EIF2AK2 dysregulation, but its precise mechanisms are yet to be clarified. In this study, we investigated the expression of EIF2AK2 in OSCC tissues and cell lines using publicly available databases and Western blotting. EIF2AK2 was silenced using small interfering RNA (siRNA), and its functional impact on OSCC malignant characteristics was determined using several in vitro experiments. Additionally, we determined EIF2AK2’s impact on autophagy levels and the activity of mechanistic pathways. Our results demonstrate that EIF2AK2 is markedly overexpressed in OSCC tissues and cell lines, and its knockdown significantly affects OSCC malignant characteristics, such as proliferation, migration, and invasion. Furthermore, EIF2AK2 knockdown increased E-cadherin levels while reducing those of N-cadherin and Vimentin, supporting EMT suppression. It also led to reduced autophagy based on decreased LC3-II and Beclin-1 and increased p62 expressions. Moreover, inhibition of EIF2AK2 led to the downregulation of the JAK2/STAT3 axis. Collectively, these findings support EIF2AK2 as an oncogene in OSCC progression by activating autophagy through the JAK2/STAT3 pathway.