ArticleInternational journal of clinical and experimental pathology2019
IGF-1R inhibitor PQ401 inhibits osteosarcoma cell proliferation, migration and colony formation.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Targeted therapy for osteosarcoma: a review.Journal of cancer research and clinical oncology · 2023Review
- Multi-Omics Immune Interaction Networks in Lung Cancer Tumorigenesis, Proliferation, and Survival.International journal of molecular sciences · 2022Article
- Article
- The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia.Frontiers in cell and developmental biology · 2021Review
- The Clinical Significance and Potential Molecular Mechanism of Upregulated CDC28 Protein Kinase Regulatory Subunit 1B in Osteosarcoma.Journal of oncology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
31933976PMC6947108W3005027176What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.