LncRNA SNHG1 negatively regulates miRNA‑101‑3p to enhance the expression of ROCK1 and promote cellproliferation, migration and invasion in osteosarcoma.

Abstract

Osteosarcoma (OS) is a rare malignant bone tumor that commonly occurs in children and adolescents and causes pain and swelling of the long bones of the legs and arms. Long non-coding RNA (lncRNA) and micro (mi)RNA-101 are important in the initialization and progression of OS. However, the mechanism underlying the role of the lncRNA and miRNA-101 in OS remains to be fully elucidated. In the present study, through reverse transcription-quantitative polymerase chain reaction analysis, it was first found that the lncRNA SNHG1 was upregulated and miRNA-101-3p was downregulated in OS tissues and cell lines. Second, the knockdown of lncRNA SNHG1 induced cell apoptosis and maintained the cell cycle at the G0/G1 phase, which decreased the overall cell viability. Furthermore, according to a dual-luciferase assay and western blot analysis, miRNA-101-3p was found to be a target of the lncRNA SNHG1 in OS, which further regulated the expression of Rho-associated coiled-coil-containing protein kinase 1 (ROCK1). It was found that the phosphoinositide 3-kinase/ATK pathway was inactivated and that epithelial-mesenchymal transition was activated in OS cell lines with overexpression of the lncRNA SNHG1. Taken together, in OS cell lines, the lncRNA SNHG1 acted as an oncogene, and miRNA-101-3p was considered a tumor suppressor. The lncRNA SNHG1 promoted OS cell proliferation, migration and invasion by downregulating the expression of miRNA-101-3p, which enhanced the expression of ROCK1.