Research articles
ScienceAsia 52 (2026): 1-10 |doi:
10.2306/scienceasia1513-1874.2026.082
ECT2 promotes proliferation and stemness of pancreatic
cancer cells via the Wnt/β-catenin signaling pathway
Chang Chena,?, Jie Lia,b,e,?, Xiaoping Tanb,d, Ziao Wanga, Qing Zhanga,b,c,e,*
ABSTRACT: Epithelial cell transformation 2 (ECT2) plays a critical role in human oncogenesis, but its biological
role in pancreatic adenocarcinoma (PAAD) remains unclear. Bioinformatics analysis was performed to evaluate the
expression of ECT2 in PAAD and its prognostic value. Functional assays and Western blot were performed to explore
the effects of ECT2 on the proliferation and stemness of pancreatic cancer cells. TCGA and GTEx databases revealed
upregulated ECT2 expression in PAAD tissues (n = 178), which was associated with advanced T3/T4 stage, deceased
status, and disease-specific survival (DSS) events (p < 0.05). Furthermore, high ECT2 expression correlated with
poor overall survival (OS), relapse-free survival (RFS), and progression-free interval (PFI) (p < 0.05). ECT2 knockout
inhibited proliferation, colony formation, and sphere formation (p < 0.05), and decreased the expression of Cyclin D1,
CDC25C, CD24, OCT4, and SOX2. Conversely, overexpression of ECT2 enhanced proliferation, colony formation, and
sphere formation (p < 0.05), and increased the expression of Cyclin D1, CDC25C, CD24, OCT4, and SOX2. Gene Set
Enrichment Analysis (GSEA) revealed that high ECT2 expression was linked to pancreatic cancer, the cell cycle, and
classical Wnt signaling. ECT2 expression was positively correlated with ?-catenin levels (R = 0.481, p < 0.001). ECT2
knockout reduced ?-catenin expression, but increased p-?-catenin, GSK-3?, and Axin1 expression. In contrast, ECT2
overexpression increased ?-catenin expression while reducing p-?-catenin, GSK-3?, and Axin1 expression. This study
revealed that ECT2 promotes the proliferation and stemness of pancreatic cancer cells via the Wnt/?-catenin signaling
pathway. ECT2 may serve as a prognostic biomarker and therapeutic target for pancreatic cancer.
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| a |
Department of Gastroenterology, First Hospital of Yangtze University, Jingzhou, Hubei 434000 China |
| b |
Digestive Disease Research Institution of Yangtze University, Jingzhou, Hubei 434000 China |
| c |
Clinical Medical College, Yangtze University, Jingzhou, Hubei 434000 China |
| d |
The Third Clinical Medical College of Yangtze University, Jingzhou Hospital of Traditional Chinese Medicine,
Jingzhou, Hubei 434000 China |
| e |
Hubei Provincial Clinical Research Center for Personalized Cancer Diagnosis and Therapy, Hubei 430000 China |
* Corresponding author, E-mail: zqcn@yangtzeu.edu.cn
Received 19 Mar 2026, Accepted 24 Jul 2026
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