CKB affects human osteosarcoma progression by regulating the p53 pathway

This study aimed to explore the role of the creatine kinase B (CKB) gene in the development of human osteosarcoma (OS). Western blotting and qRT-PCR were performed to detect CKB expression in tissues and cells. CCK-8, colony formation, flow cytometry, Transwell, and cell scratch assays were performed to detect OS cell viability, proliferation, apoptosis, invasion, and migration. Gene set enrichment analysis (GSEA) was used to conduct signal pathway enrichment. CKB expression was higher in OS tissues and cells than that in normal tissues and cells. Silencing CKB expression reduced cell proliferation, migration, and invasion, and improved cell apoptosis in HOS cells, while overexpressing CKB increased cell proliferation, migration, and invasion, and decreased apoptosis in U2-OS cells. GSEA showed that CKB affected the p53 signaling pathway. Overexpression of CKB inhibited the protein expression of p53, p21, and Bax and promoted the expression of Bcl-2 and MDM2 in U2-OS cells. Conversely, silencing CKB promoted the protein expression of p53, p21, and Bax, and inhibited the expression of Bcl-2 and MDM2 in HOS cells. Silencing p53 could reverse the effect of the silencing CKB in HOS cells, and overexpressing p53 could reverse the effect of overexpressing CKB in U2-OS cells. Taken together, CKB affects the development of OS by regulating the activity of the p53 signaling pathway.