The splicing factor proline and glutamine rich promotes the growth of osteosarcoma via the c-Myc signaling pathway

Splicing factor proline- and glutamine-rich (SFPQ) regulates transcripts in skeletal muscle metabolism and tumorigenesis. As osteosarcoma (OS) is the most common malignant bone tumor characterized by genome instability, such as MYC amplification, this study aimed to investigate the role and mechanism of SFPQ in OS. Expression of SFPQ in OS cell lines and human OS tissues was detected using quantitative real-time PCR, western blot, and fluorescence in situ hybridization (FISH) analyses. The oncogenic role of SFPQ in OS cells and murine xenograft models and the underlying mechanism of SFPQ on the c-Myc signaling pathway were assessed in vitro and in vivo. Results showed that SFPQ expression was upregulated and correlated with poor prognosis in OS patients. SFPQ overexpression promoted the malignant biological behavior of OS cells, while its knockdown markedly reduced the oncogenic function of OS. Additionally, depletion of SFPQ inhibited OS growth and bone destruction in nude mice. SFPQ overexpression induced malignant biological behaviors, which could be rescued by the depletion of c-Myc. These results suggest an oncogenic role of SFPQ in OS, possibly through the c-Myc signaling pathway.