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An Orthotopic Resectional Mouse Model of Pancreatic Cancer
Published on: September 24, 2020
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Targeting CXCL5 in Pancreatic Cancer Cells Inhibits Cancer Xenograft Growth by Reducing Proliferation and Inhibiting
Zheng-Zheng Wang1, Xiao-Ting Li2, Qing-Jun Li1
1Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, Zhengzhou, 450008, China.
Digestive Diseases and Sciences
|June 1, 2022
Summary
High levels of C-X-C ligand 5 (CXCL5) in pancreatic cancer (PC) correlate with poor prognosis and promote tumor growth and migration. Inhibiting CXCL5 may offer a new therapeutic strategy for pancreatic cancer.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Pancreatic cancer (PC) is a highly lethal malignancy with poor survival rates.
- C-X-C ligand 5 (CXCL5) is a chemokine implicated in various cancers, but its role in PC progression is unclear.
Purpose of the Study:
- To investigate the role and prognostic significance of CXCL5 in pancreatic cancer progression.
Main Methods:
- Analyzed CXCL5 expression in PC tissues and cell lines using databases, immunohistochemistry, and Western blotting.
- Conducted in vitro experiments to assess the impact of CXCL5 on PC cell proliferation, migration, and epithelial-mesenchymal transition (EMT).
- Performed in vivo xenograft studies to evaluate the effect of CXCL5 knockdown on tumor growth.
Main Results:
- CXCL5 expression is significantly elevated in PC tissues and correlates with poor patient prognosis.
- Overexpression of CXCL5 enhances PC cell proliferation, migration, and EMT markers (SNAI2, TWIST1).
- Knockdown of CXCL5 inhibits PC cell growth, migration, and EMT in vitro and reduces tumor growth in vivo.
Conclusions:
- High CXCL5 expression is a predictor of poor prognosis in pancreatic cancer patients.
- CXCL5 promotes pancreatic cancer cell growth and EMT.
- Targeting CXCL5 presents a potential therapeutic strategy for pancreatic cancer.

