Scholarlink

Background <p>Ewing sarcoma (EWS) is a highly aggressive and poorly differentiated malignancy. Despite its high metastatic potential, the molecular mechanisms underlying EWS metastasis remain largely unclear.</p> Methods <p>Differentially expressed genes (DEGs) between metastatic and primary EWS were identified by analyzing the GSE12102 dataset. A protein-protein interaction (PPI) network was constructed to identify hub genes. The expression levels of hub genes were validated in RD-ES and SK-N-MC cells using RT-qPCR and western blot. Wound healing and Transwell invasion assays were performed to evaluate cell migration and invasion. The PI3K activator 740Y-P was used to determine whether PI3K/AKT pathway activation was involved in EpCAM-mediated malignant phenotypes.</p> Results <p>A total of 1,183 genes were identified as DEGs. RT-qPCR and western blot analyses demonstrated that the expression levels of EpCAM, GATA6, and CFTR were higher in metastasis-derived Ewing family tumor cell line SK-N-MC than in the primary EWS cell line RD-ES. EpCAM knockdown inhibited the migration and invasion of SK-N-MC cells. Mechanistically, EpCAM silencing reduced the p-PI3K/PI3K and p-AKT/AKT ratios. Treatment with 740Y-P activated the PI3K/AKT pathway, promoted SK-N-MC cell viability, migration, and invasion, and partially reversed the inhibitory effects induced by EpCAM knockdown.</p> Conclusion <p>Our findings suggest that EpCAM may promote the migration, invasion, and metastasis potential of EWS through activation of the PI3K/AKT signaling pathway. These findings provide new insights into the molecular mechanisms underlying EWS metastasis.</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

EpCAM promotes metastasis-associated phenotypes in Ewing sarcoma-family tumor cells by activating the PI3K/AKT signaling pathway

  • 期刊论文

  • 发表日期：

    2026年6月3日

查看全文
  • Bin Deng,
  • Shengcheng Yao,
  • Shaosong Sun,
  • Xingchen Zhang,
  • Kaijin Guo

摘要

Background

Ewing sarcoma (EWS) is a highly aggressive and poorly differentiated malignancy. Despite its high metastatic potential, the molecular mechanisms underlying EWS metastasis remain largely unclear.

Methods

Differentially expressed genes (DEGs) between metastatic and primary EWS were identified by analyzing the GSE12102 dataset. A protein-protein interaction (PPI) network was constructed to identify hub genes. The expression levels of hub genes were validated in RD-ES and SK-N-MC cells using RT-qPCR and western blot. Wound healing and Transwell invasion assays were performed to evaluate cell migration and invasion. The PI3K activator 740Y-P was used to determine whether PI3K/AKT pathway activation was involved in EpCAM-mediated malignant phenotypes.

Results

A total of 1,183 genes were identified as DEGs. RT-qPCR and western blot analyses demonstrated that the expression levels of EpCAM, GATA6, and CFTR were higher in metastasis-derived Ewing family tumor cell line SK-N-MC than in the primary EWS cell line RD-ES. EpCAM knockdown inhibited the migration and invasion of SK-N-MC cells. Mechanistically, EpCAM silencing reduced the p-PI3K/PI3K and p-AKT/AKT ratios. Treatment with 740Y-P activated the PI3K/AKT pathway, promoted SK-N-MC cell viability, migration, and invasion, and partially reversed the inhibitory effects induced by EpCAM knockdown.

Conclusion

Our findings suggest that EpCAM may promote the migration, invasion, and metastasis potential of EWS through activation of the PI3K/AKT signaling pathway. These findings provide new insights into the molecular mechanisms underlying EWS metastasis.