CircPARD3 promotes osteosarcoma proliferation and metastasis through regulating the miRNA-1294/ SKIL Pathway

Background: Osteosarcoma (OS) is the most common malignant bone tumor in the pediatric population. The main goal of this study is to investigate the role of circPARD3 and the underlying signaling pathway involved in OS.Methods: Cell proliferation was measured using a CCK-8 assay kit and clone formation assay. Cell migration and invasion was measured using transwell assay kit and wound-healing assay. Change of RNA and protein expression was determined using RNA extract and quantitative real time PCR (RT-qPCR) assay and Western blotting, respectively. RNA immune precipitation and Luciferase assay was used to confirm the predicted results. The xenograft model was established to evaluate the function of circPARD3 in vivo.Results: Expression of circPARD3 was upregulated in both OS tissues and cell lines. Silencing circPARD3 repressed OS cell proliferation and metastasis, while overexpression of circPARD3 promote OS cell tumorigenesis in vitro. Furthermore, up-regulation of circPARD3 significantly promoted the growth of OS cells in vivo. Moreover, circPARD3 directly and negatively modulated the expression of miR-1294 and positively regulated the expression of SKIL. Conclusion: Abnormally high expression of circPARD3 may promote the proliferation, migration, and invasion of OS cells through up-regulating SKIL by sponging miR-1294. These results provide insight into therapeutic targets for preventing and treating OS.