miR-1290 inhibits chordoma cell proliferation and invasion by targeting Robo1

Background: Chordoma is a low-grade aggressive bone tumor with a high local recurrence. MicroRNAs (miRNAs) have been reported to play crucial roles in the development of chordoma. Our previous study has shown miR-1290 is associated with muscle invasion and the prognosis of chordoma. However, the underlying mechanism of miR-1290 in chordoma remains unclear. In this study, we aimed to explore the function of miR-1290 in the biological behaviors of chordoma. Methods: Sixteen sacral chordoma samples and 10 fetal nucleus pulposus specimens were collected for the detection of miR-1290 and Robol at the First Affiliated Hospital of Soochow University. Bioinformatic analysis and a luciferase reporter assay was used to verify the interaction between miR-1290 and the target gene robol in chordoma. Effects of miR-1290 expression on chordoma cell proliferation and invasion were explored by clone formation and Transwell assay in vitro. The underlying mechanisms of miR-1290 and Robol in chordoma cell proliferation and invasion were also explored in the U-CH 1 cell line. Results: In vitro functional analysis, including clone formation, and Transwell assays indicated overexpression of miR-1290 significantly suppressed chordoma cell proliferation and invasion. Bioinformatic analysis revealed Robol as a potential target of tniR-1290, and luciferase reporter assays demonstrated the association between miR-1290 and the Robol gene in U-CH I cells. Robol was further confirmed to be up-regulated in chordoma tissues by immunohistochemistry (IHC), which is negatively correlated with miR-1290 expression in chordoma tissue. Additionally, we found down-regulation of miR-1290 could induce the expression of Robol in chordoma cells, while the elevation of miR-1290 expression could inhibit Robol expression in chordoma cells. Conclusions: miR-1290 inhibits chordoma cell proliferation and invasion by negatively regulating the Robo1 gene.