ArticleBMC cancer2017
Therapeutic potential of TAS-115 via c-MET and PDGFRα signal inhibition for synovial sarcoma.
Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Medicinal Chemistry of Small-Molecule c-Met Inhibitors: From Approved Therapies to Emerging Multitarget Anticancer Agents.International journal of molecular sciences · 2026Review
- Cooperative Roles of Class IA PI3K Isoforms in Translocation-Related Sarcoma Cell Survival and Proliferation.Cancer research communications · 2026Article
- Drug-drug interactions with pioglitazone, losartan, and midazolam and anti-tumor efficacy and safety study of TAS-115 in patients with solid tumors.Cancer chemotherapy and pharmacology · 2026Article
- Therapeutic potential of TAS-115 in 3D breast cancer models.Biofabrication · 2025Article
- Comparative Characterization of Tumor Microenvironments in Monophasic and Biphasic Synovial Sarcomas.International journal of molecular sciences · 2025Article
- Establishment and characterization of NCC-SS6-C1: a novel patient-derived cell line of synovial sarcoma.Human cell · 2024Article
- Genetic and Molecular Heterogeneity of Synovial Sarcoma and Associated Challenges in Therapy.Cells · 2024Review
- Xenografting Human Musculoskeletal Sarcomas in Mice, Chick Embryo, and Zebrafish: How to Boost Translational Research.Biomedicines · 2024Review
- TAS-115 inhibits PDGFRα/AXL/FLT-3 signaling and suppresses lung metastasis of osteosarcoma.FEBS open bio · 2020Article
- Another Weapon in the Battle against Idiopathic Pulmonary Fibrosis?American journal of respiratory cell and molecular biology · 2019Article
- Article
- Safety and Tolerability of c-MET Inhibitors in Cancer.Drug safety · 2019Review
- Primary poorly differentiated monophasic synovial sarcoma of ileum mesenteries with pulmonary metastasis: a case report.International journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe prognosis of synovial sarcoma (SS), an aggressive soft tissue sarcoma, remains poor. We previously reported that c-MET or platelet-derived growth factor receptor α (PDGFRα) signalling pathway is related to SS progression based upon the findings of phospho-receptor tyrosine kinase (RTK) arrays. TAS-115 is a novel c-MET/ vascular endothelial growth factor receptor-targeting tyrosine kinase inhibitor that has been shown to inhibit multiple RTKs. Here we aimed to investigate the therapeutic potential of TAS-115 against SS.
methodsWe first evaluated which signalling pathway was relevant to the viability of three human SS cell lines: Yamato-SS, SYO-1 and HS-SY-II. Next, we assessed the anticancer activity and mechanism of action of TAS-115 in these SS cell lines. Finally, we compared the ability of TAS-115 to inhibit c-MET and PDGFRα phosphorylation with that of pazopanib.
resultsWe classified the SS cell lines as c-MET-dependent or PDGFRα-dependent based upon the differences in the signalling pathway relevant for growth and/or survival. We also found that c-MET and PDGFRα were the primary activators of both phosphatidylinositol 3-kinase/AKT and mitogen-activated protein kinase pathways in c-MET-dependent and PDGFRα-dependent SS cells, respectively. TAS-115 treatment blocked the phosphorylation of PDGFRα as well as that of c-MET and their downstream effectors, leading to marked growth inhibition in both types of SS cell lines in in vitro and in vivo studies. Furthermore, PDGFRα phosphorylation, on at least four representative autophosphorylation sites, was impeded by TAS-115 equivalently to pazopanib.
conclusionsThese experimental results have demonstrated the significance of c-MET and PDGFRα signalling for growth and/or survival of SS tumours. TAS-115 monotherapy may benefit SS patients whose tumours are dependent upon either c-MET or PDGFRα signalling by functioning as a multiple tyrosine kinase inhibitor to suppress c-MET as well as PDGFRα pathways.
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