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Updated: Feb 5, 2026

Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells
Published on: May 2, 2017
uPAR Is Regulated via miR-561-3p and Affects the Progression and Aggressiveness of CRC Cells
Xi Yang1, Xuelian Wang2, Lu Sang2
1Department of Clinical Laboratory, Beijing Huairou Hospital, Beijing, China sunrise0312@126.com.
Objective:
Urokinase plasminogen activator (uPA), its receptor uPAR, and plasminogen activator inhibitor type 1 (PAI-1), constitute the plasminogen urokinase activation system that is thought to be associated with the malignant biology of cancer cells. Nevertheless, the regulation mechanism of uPAR expression in colorectal cancer remains unclear.
Methods:
The effect of uPAR and miR-516-3p on CRC cells was explored through Methyl thiazolyl tetrazolium (MTT) assay, colony formation, Transwell, and Apoptosis assays. Dual-luciferase reporter assays, reverse transcription quantitative PCR (RT-qPCR), and Western blot assay were carried out to determine that uPAR is directly regulated by miR-561-3p. Levels of protein expression were analyzed by Western blot assay.
Results:
In the study, we showed that uPAR was upregulated in serum samples from CRC patients and associated with the more advanced stage and distant metastasis in patients with CRC. In CRC cells, uPAR promotes cell growth, migration, and invasion, while inhibiting cell apoptosis. In addition, the expression of uPAR is negatively regulated by miR-561-3p through binging its 3' UTR.
Conclusion:
uPAR is downregulated by miR-561-3p, contributing to tumorigenesis in colorectal cancer.
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