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Updated: Dec 31, 2025
Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
Published on: October 28, 2021
IGF-1R inhibitor PQ401 inhibits osteosarcoma cell proliferation, migration and colony formation
Baochang Qi1, Riping Zhang2, Rujun Sun3
1Department of Orthopedics, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, Heilongjiang, China.
Abstract:
IGF-1R is expressed abnormally in osteosarcoma (OS) and could participate in its progression. In this study, we aimed to explore the effect of the IGF-1R inhibitor PQ401 as a treatment for OS. The relative expression of IGF-1R in OS patient tumors and the U2OS cell line were determined by qRT-PCR and by accessing information in a public database. Inhibition of cell proliferation by PQ401 was determined by MTT assay. Cell migration under low concentration treatment of PQ401 was carried out by transwell and wound healing assays. PQ401 induction of OS cell apoptosis was investigated by flow cytometry. Tumorigenesis under PQ401 treatment was evaluated by a colony formation assay. Finally, downstream blockage of the IGF-1R pathway was verified by western blotting. Our results show that the expression of IGF-1R was remarkably higher in OS cells, particularly in U2OS, than in other cancer-type cell lines. The inhibition of the IGF-1R pathway by PQ401 exhibited significant anticancer activity in the U2OS cell line in not only proliferation but also migration and colony formation. In addition, PQ401 is a strong inducer of OS cell apoptosis. Furthermore, western blotting was used to demonstrate that the IGF-1R related downstream pathway, including total ERK1/2, was significantly inhibited by PQ401. Thus, IGF-1R inhibition may represent a novel treatment for OS.
Insights
The insulin-like growth factor 1 receptor (IGF-1R) inhibitor PQ401 shows significant potential in treating osteosarcoma (OS). PQ401 effectively inhibits OS cell proliferation, migration, and colony formation while inducing apoptosis, suggesting a novel therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Insulin-like growth factor 1 receptor (IGF-1R) is abnormally expressed in osteosarcoma (OS), suggesting its role in disease progression.
- Targeting IGF-1R presents a potential therapeutic avenue for OS treatment.
Purpose of the Study:
- To investigate the therapeutic effects of the IGF-1R inhibitor PQ401 on osteosarcoma.
- To evaluate PQ401's impact on OS cell proliferation, migration, apoptosis, and tumorigenesis.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and public database analysis to assess IGF-1R expression.
- MTT assays for proliferation, transwell and wound healing assays for migration, flow cytometry for apoptosis, and colony formation assays for tumorigenesis.
- Western blotting to verify downstream pathway inhibition.
Main Results:
- IGF-1R expression was significantly higher in OS cells, particularly U2OS, compared to other cancer cell lines.
- PQ401 demonstrated significant anticancer activity by inhibiting proliferation, migration, and colony formation in U2OS cells.
- PQ401 effectively induced apoptosis in OS cells and inhibited the downstream IGF-1R pathway, including ERK1/2.
Conclusions:
- IGF-1R inhibition using PQ401 exhibits potent anticancer effects against osteosarcoma.
- PQ401 demonstrates multifaceted therapeutic potential by targeting proliferation, migration, and inducing apoptosis.
- Targeting the IGF-1R pathway with PQ401 represents a promising novel treatment strategy for osteosarcoma.
