Background The prognosis of synovial sarcoma (SS), an aggressive soft tissue sarcoma, remains poor. respectively. TAS-115 treatment blocked the phosphorylation of PDGFR 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, PDGFR phosphorylation, on at least four representative autophosphorylation sites, was impeded by TAS-115 equivalently to pazopanib. Conclusions These experimental results have demonstrated the significance of c-MET and PDGFR 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 PDGFR signalling by functioning as a multiple tyrosine kinase inhibitor to suppress c-MET as well as PDGFR pathways. Electronic supplementary material The online version of this article 17374-26-4 IC50 (doi:10.1186/s12885-017-3324-3) contains supplementary material, which is available to authorized users. proto-oncogene, is known to be a hepatocyte growth factor (HGF) receptor [9]. Activation of the HGF/c-MET axis in cancer has been reported to be involved in cellular proliferation, survival, migration and angiogenesis [10]. We have found that a selective c-MET inhibitor suppresses the growth of Yamato-SS cells, but fails to suppress the growth of SYO-1 or HS-SY-II cells [11]. PDGFR and PGDFR signalling indirectly promotes tumour development by activating the mesenchymal cells in the tumour microenvironment and directly stimulates the growth of malignant cells [12]. Pazopanib, a PDGFR/ vascular endothelial growth factor receptor (VEGFR)/ c-kit (stem cell factor receptor) inhibitor [13], is the only tyrosine kinase inhibitor approved for advanced soft 17374-26-4 IC50 tissue sarcomas in Japan. Hosaka et al. showed that pazopanib 17374-26-4 IC50 suppressed the growth of SYO-1 and HS-SY-II cells through inhibition of the PDGFR and phosphatidylinositol 3-kinase (PI3K)/AKT pathways [14]. Based upon these studies, we hypothesize that inhibition of the c-MET or PDGFR signalling pathway would be a therapeutic strategy for the treatment of SS. TAS-115, a novel c-MET/VEGFR-targeting tyrosine kinase inhibitor that exerts its effect via ATP antagonism, has been reported to inhibit multiple RTKs [15]. Recently, it was reported that TAS-115 had a 17374-26-4 IC50 favourable tolerability profile and exhibited antitumour activity in human gastric cancer [15, 16] and in human lung cancer [17, 18] via inhibition of c-MET/VEGFR signalling. However, the efficacy of this drug for soft tissue sarcomas remains unclear. In the present study, we first evaluated the phosphorylation status of RTKs in three human SS cell lines, Yamato-SS, SYO-1 and HS-SY-II, and then investigated which RTK was critical for the viability of each of these cell lines. Next, we tested the antitumour activity and the mechanism of action of TAS-115 in these SS cells. Finally, we compared the inhibitory activity of TAS-115 on the c-MET and PDGFR pathways with that of pazopanib. On the basis of our observations, we discuss the potential clinical value of TAS-115 monotherapy, via c-MET and PDGFR signal inhibition, in patients with SS. Methods Cell lines The Yamato-SS cell line was established from surgically resected tumours in our laboratory, as previously described MAP3K11 [19]. SYO-1 was kindly supplied by Dr. Ozaki (Okayama University, Okayama, Japan) [20]. HS-SY-II [21] was provided by the RIKEN BRC (Tsukuba, Japan) through the National Bio-Resource Project of the MEXT, Japan. We authenticated Yamato-SS and HS-SY-II through short tandem repeat inspection. SYO-1 was confirmed by the expression of the fusion gene by reverse transcription polymerase chain reaction. Yamato-SS and SYO-1 cells originally derived.