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Updated: Jun 9, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
EpCAM promotes metastasis-associated phenotypes in Ewing sarcoma-family tumor cells by activating the PI3K/AKT
Bin Deng1, Shengcheng Yao2, Shaosong Sun2
1Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, 211166 Jiangsu China.
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.
Supplementary Information:
The online version contains supplementary material available at 10.1007/s10616-026-01001-y.
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