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Updated: Jun 9, 2026

Ultrasound-Guided Orthotopic Implantation of Murine Pancreatic Ductal Adenocarcinoma
Published on: November 19, 2019
CXCL10 drives pancreatic ductal adenocarcinoma progression through CXCR3-ERK/MAPK signaling
Haomin Yuan1, Longhang Wu1, Yu Song1
1Department of General Surgery, Union Hospital of Fujian Medical University, Fuzhou 350001, Fujian, China.
Abstract:
The functional significance of the CXCL10/CXCR3 chemokine axis in pancreatic ductal adenocarcinoma (PDAC) remains incompletely defined. Through integrated analysis of clinical datasets, patient samples, and functional assays, we demonstrate that CXCL10 and CXCR3 are frequently overexpressed in PDAC, with high levels correlating with advanced disease and poorer overall survival. Notably, CXCR3 expression emerged as an independent prognostic indicator. Functionally, CXCL10 treatment or overexpression enhanced PDAC cell proliferation, migration, invasion, clonogenicity, and epithelial-mesenchymal transition (EMT). Conversely, CXCL10 knockdown or pharmacological CXCR3 inhibition with AMG487 suppressed these oncogenic phenotypes. Mechanistically, CXCL10 signaling activated the ERK/MAPK pathway, and ERK inhibition abolished its tumor-promoting effects. This study establishes that CXCL10 drives PDAC progression through CXCR3-dependent ERK/MAPK activation, positioning this axis as a potential therapeutic target.
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