LINC01060 knockdown inhibits osteosarcoma cell malignant behaviors in vitro and tumor growth and metastasis in vivo through the PI3K/Akt signaling

Abstract

Despite its low frequency, osteosarcoma is one of the deadliest malignancies in children and adolescents. The phosphatidylinositol 3-kinase (PI3K)/Akt signaling activation and epithelial-to-mesenchymal transition (EMT) are critical issues during osteosarcoma development. This study found long intergenic non-protein coding RNA 1060 (LINC01060) to be an EMT-related long non-coding RNA (lncRNA) up-regulated in osteosarcoma; higher LINC01060 expression was linked to a worse prognosis in osteosarcoma patients. In vitro, knocking down LINC01060 significantly inhibits osteosarcoma cell malignant behaviors, including hyperproliferation, invasion, migration, and EMT. In vivo, LINC01060 knockdown inhibited tumor growth and metastasis, and suppressed PI3K and Akt phosphorylation. In osteosarcoma cells, Akt agonist SC79 exerted opposite effects to those of LINC01060 knockdown through the promotion of cell viability, cell migration, and cell invasion. Moreover, the Akt agonist SC79 partially eliminated LINC01060 knockdown effects on osteosarcoma cells, suggesting that LINC01060 exerts its effects through the PI3K/Akt signaling. Therefore, it is deduced that LINC01060 is overexpressed in osteosarcoma. In vitro, LINC01060 knockdown inhibits cancer cell malignant behaviors; in vivo, LINC01060 knockdown inhibits tumor development and metastasis. The PI3K/Akt signaling is involved in LINC01060 functions in osteosarcoma.

Keywords

• osteosarcoma
• the pi3k/akt signaling
• epithelial-to-mesenchymal transition (emt)
• metastasis
• linc01060