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Updated: Dec 25, 2025
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-520d-5p functions as a tumor-suppressor gene in cervical cancer through targeting PTK2
Li Zhang1, Fuwei Liu2, Yajie Fu3
1Department of Gynecology, The Maternal and Child Health Hospital of Zibo City, Zibo City, Shandong 255029, China.
Objective:
PTK2 has been reported to be involved in tumor progression, but its regulating mechanisms in cervical cancer (CC) remain to be elusive. MiRNA-520d-5p was demonstrated to regulate the expression of many genes and inhibit the development of human tumors. However, the functional mechanisms of miRNA-520d-5p in the regulation of cervical cancer are not fully understood.
Methods:
RT-qPCR was employed to detect the expression levels of miR-520d-5p and PTK2. Western blot was performed to detect the expression levels of proteins. Dual-luciferase reporter assay was utilized to investigate the associations between miR-520d-5p and PTK2. CCK-8 assay was carried out to measure cell proliferation. In addition, transwell assay and scratch assay were used for cell invasion and migration analysis. Flow cytometry was used to detect cell apoptosis of cervical cancer.
Results:
The expression levels of PTK2 were elevated in CC tissues and cells lines. It was found that PTK2 was a target gene of miR-520d-5p. The expression of miR-520d-5p was down-regulated in CC tissues, which was negatively correlated with the expression of PTK2. MiR-520d-5p inhibited the proliferation, migration, and invasion of CC cells. In addition, overexpression of miR-520d-5p resulted in apoptosis of CC cells. Finally, we demonstrated that miR-520d-5p inhibited the activation of PI3K/AKT signaling.
Conclusion:
MiR-520d-5p suppressed the proliferation, invasion, and migration of CC cells via targeting PTK2.
Insights
MicroRNA-520d-5p suppresses cervical cancer (CC) progression by targeting PTK2. This microRNA inhibits CC cell proliferation, migration, and invasion, offering potential therapeutic strategies for cervical cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- PTK2 is implicated in tumor progression, but its role in cervical cancer (CC) is unclear.
- MicroRNA-520d-5p (miR-520d-5p) is known to inhibit tumor development, yet its specific mechanisms in CC require elucidation.
Purpose of the Study:
- To investigate the regulatory role of miR-520d-5p in cervical cancer.
- To determine the relationship between miR-520d-5p and PTK2 in CC.
- To explore the functional impact of miR-520d-5p on CC cell behavior and signaling pathways.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) for gene and microRNA expression analysis.
- Western blot for protein level detection.
- Dual-luciferase reporter assay to confirm direct targeting.
- Cell Counting Kit-8 (CCK-8), Transwell, and scratch assays for proliferation, invasion, and migration.
- Flow cytometry for apoptosis analysis.
Main Results:
- PTK2 expression was elevated in CC tissues and cell lines.
- miR-520d-5p was downregulated in CC and inversely correlated with PTK2 expression.
- miR-520d-5p significantly inhibited CC cell proliferation, migration, and invasion.
- Overexpression of miR-520d-5p induced apoptosis in CC cells.
- miR-520d-5p suppressed the PI3K/AKT signaling pathway.
Conclusions:
- miR-520d-5p acts as a tumor suppressor in cervical cancer.
- miR-520d-5p targets PTK2 to inhibit CC cell proliferation, invasion, and migration.
- These findings highlight miR-520d-5p as a potential therapeutic target for cervical cancer.
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