Abstract
Osteosarcoma is a malignancy with high aggressiveness and poor prognosis, which occurs mainly in children. The therapeutic strategy against osteosarcoma includes surgery combined with chemotherapy and radiotherapy. Although the treatment of osteosarcoma has been improved in recent years, there is a large proportion of patients with incurable osteosarcoma. Investigation of the mechanism of osteosarcoma progression would be of great help in discovering therapeutic targets for this disease. Long non-coding RNAs play critical roles in the pathogenesis of different types of cancer. The current study showed that long non-coding RNA NR_027471 was downregulated in osteosarcoma cells. In vitro and in vivo studies indicated that upregulation of NR_027471 impeded the viability, proliferation, and invasion of osteosarcoma, as well as induced cell cycle arrest at G1. In addition, binding of miR-8055 to NR_027471 was demonstrated, thereby influencing the expression of tumor protein p53 inducible nuclear protein 1 (TP53INP1). Knockdown of NR_027471 promoted epithelial–mesenchymal transition by inhibiting E-cadherin and increasing the expression of zinc finger E-box-binding homeobox 1 (ZEB1), Snail, and fibronectin. These results suggested that overexpression of NR_027471 upregulated TP53INP1 by sponging to miR-8055, leading to suppression of osteosarcoma cell proliferation and progression.
Highlights
Osteosarcoma is the most common malignancy of bone [1]
The results indicated that NR_027471 was significantly downregulated in osteosarcoma cell lines (U2OS, Saos-2, MG-63, and HOS) compared with hFOB1.19, Human foreskin fibroblast-1 (HFF-1), and human bone marrow stem cells (hBMSCs) (Figure 1B)
Cell Counting Kit-8 (CCK-8) analysis showed that osteosarcoma cell viability was suppressed at 48, 72, and 96 h when lncRNA NR_027471 was overexpressed compared to pLVX-Vector group and osteosarcoma cell viability was upregulated at 48, 72, and 96 h with lncRNA NR_027471 knockdown compared to pLKO.1group (Figure 2B)
Summary
Osteosarcoma is the most common malignancy of bone [1]. It is predominantly diagnosed in children and adolescents aged 10–25 years [2]. The current treatment of osteosarcoma involves the combination of surgical resection with radiotherapy and chemotherapy. The treatment of osteosarcoma has improved in recent years, the survival rate and prognosis of such patients remain poor [3]. Identification of the mechanisms underlying the progression of osteosarcoma would help to find promising therapeutic strategies and ameliorate clinical outcomes.
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