Related Experiment Video
Updated: Jan 20, 2026

Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
Published on: October 28, 2021
miR-627-3p inhibits osteosarcoma cell proliferation and metastasis by targeting PTN
Ming He1, Peng Shen1, Chuang Qiu1
1Department of Orthopedic Surgery, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.
Abstract:
Dysregulation of microRNA (miRNA) has been observed in several types of tumors, including osteosarcoma. Biochip analysis was used to identify miRNAs differentially expressed in osteosarcoma tissues. The targeting sites of miR-627-3p were analyzed using miRDB software and fluorescein reporter gene. MTT and Transwell assays were used to analyze the effects of miR-627-3p on the growth and migration of osteosarcoma cells. Western blotting and real-time PCR were used to detect the effects of miR-627-3p on related proteins. In vivo experiments were conducted to verify the effect of miR-627-3p on osteosarcoma. We focused on miR-627-3p because it was the most significantly downregulated miRNA in our screening study. Through luciferase reporter assays, western blotting and real-time PCR we found that miR-627-3p directly targets PTN, and that expression levels of miR-627-3p and PTN are negatively correlated in osteosarcoma cells. Downregulation of miR-627-3p promoted osteosarcoma cell proliferation and metastasis, while its overexpression had the opposite effect. By targeting PTN, miR-627-3p also suppressed expression of Cyclin D1 and MMP2. MiR-627-3p inhibited osteosarcoma metastasis in vivo. Thus, miR-627-3p may be a useful therapeutic target for the treatment osteosarcoma or prevention of metastasis.
Insights
MicroRNA (miRNA) dysregulation is linked to osteosarcoma. This study found that miR-627-3p, a downregulated miRNA, inhibits osteosarcoma cell growth and metastasis by targeting PTN, offering a potential therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA (miRNA) dysregulation is implicated in various cancers, including osteosarcoma.
- Identifying specific miRNAs involved in osteosarcoma progression is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of miR-627-3p in osteosarcoma.
- To determine the molecular mechanisms by which miR-627-3p affects osteosarcoma cell behavior.
- To evaluate miR-627-3p as a potential therapeutic target for osteosarcoma.
Main Methods:
- Biochip analysis to identify differentially expressed miRNAs in osteosarcoma tissues.
- Bioinformatics (miRDB) and luciferase reporter assays to predict and validate miRNA targets.
- In vitro assays (MTT, Transwell) to assess cell proliferation and migration.
- Western blotting and real-time PCR to analyze protein and gene expression.
- In vivo experiments in mouse models to confirm therapeutic effects.
Main Results:
- miR-627-3p was significantly downregulated in osteosarcoma tissues.
- miR-627-3p directly targets Pleiotrophin (PTN).
- Downregulation of miR-627-3p promotes osteosarcoma cell proliferation and metastasis by upregulating PTN, Cyclin D1, and MMP2.
- Overexpression of miR-627-3p inhibits osteosarcoma cell growth and metastasis.
- miR-627-3p demonstrated inhibitory effects on osteosarcoma metastasis in vivo.
Conclusions:
- miR-627-3p acts as a tumor suppressor in osteosarcoma.
- Targeting PTN by miR-627-3p is a key mechanism in controlling osteosarcoma progression.
- miR-627-3p holds potential as a therapeutic agent for osteosarcoma treatment and metastasis prevention.
More Related Videos
Related Concept Videos
Feedback Inhibition
Cells Coordinate Growth and Proliferation
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Abnormal Proliferation
Enzyme Inhibition
Inhibition of Cdk Activity

