The type-III sodium-dependent phosphate transporters, SLC20A1 and SLC20A2, are distributed throughout the body, including the central nervous system. Various neurodegenerative diseases, including primary basal ganglia calcification (PBGC), involve the disruption of phosphate homeostasis. Patients with PBGC harbor a mutated SLC20A2. Previously, we demonstrated that the phosphate transport activity of SLC20A2 was involved in PBGC pathology. Thus, we hypothesized the activation of phosphate transport as one of the therapeutic targets for PBGC. It was previously reported that SLC20A1 and SLC20A2 were increased at vascular smooth muscle cell of ATF4-overexpression mice. This study investigated the effect of TIC10/ONC201, a potential activator of ATF4, on phosphate transport in SH-SY5Y, a neuronal cell model. Treatment with 3 µM TIC10, which did not cause cell death, increased phosphate uptake along with the ATF4 and SLC20A1 but not SLC20A2. Treatment with 3 µM TIC10 also enhanced phosphate uptake in SLC20A2-knockdowned cells but not SLC20A1-knockdowned cells. In conclusion, TIC10 enhanced phosphate uptake in SH-SY5Y cells via SLC20A1 but not SLC20A2.