MicroRNA-493-5p inhibits proliferation and metastasis of osteosarcoma cells by targeting Kruppel-like factor 5.

Osteosarcoma, including spinal osteosarcoma, has properties of high degree of malignancy, high rate of recurrence, and high incidence of metastasis. microRNAs can exert oncogenic or tumor suppressive roles in cancer cells. This study explored the effects of microRNA-493-5p (miR-493-5p) on osteosarcoma cell viability, migration, invasion, and apoptosis, as well as the underlying possible mechanism. First, the expression of miR-493-5p in osteosarcoma tissues and cells was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Then, the effects of miR-493-5p overexpression (or suppression) on osteosarcoma cell viability, migration, invasion, and apoptosis, as well as Kruppel-like factor 5 (KLF5) expression, were assessed using the Cell Counting Kit-8 assay, two-chamber transwell assay, Annexin V-FITC/PI apoptosis detection kit, qRT-PCR, and western blotting, respectively. Finally, the roles of KLF5 in miR-493-5p suppression-induced U20S cell viability, migration, and invasion enhancement, as well as the PI3K/AKT pathway activation, were evaluated. We found that miR-493-5p had lower expression in tumor tissues of spinal osteosarcoma and osteosarcoma cells. Overexpression of miR-493-5p inhibited osteosarcoma U20S cell viability, migration, and invasion, but induced cell apoptosis. On the contrary, suppression of miR-493-5p-promoted U20S cell viability, migration, and invasion. KLF5 was a direct target gene of miR-493-5p, which participated in the effects of miR-493-5p on U20S cell viability, migration, invasion, and apoptosis. Furthermore, suppression of the miR-493-5p activated PI3K/AKT pathway in U20S cells by upregulating KLF5. In conclusion, we revealed that miR-493-5p exerted tumor suppressive roles in spinal osteosarcoma and osteosarcoma cells. Overexpression of miR-493-5p inhibited proliferation and metastasis of osteosarcoma cells by downregulating KLF5 and inactivating the PI3K/AKT signaling pathway.