Long non‑coding RNA small nucleolar RNA host gene 1 knockdown suppresses the proliferation, migration and invasion of osteosarcoma cells by regulating microRNA‑424‑5p/FGF2 in vitro

Abstract

The aim of the present study was to clarify the effect of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) on the proliferation, migration and invasion of osteosarcoma (OS) cells and to explore the potential underlying mechanisms. The expression levels of SNHG1, microRNA (miR)-424-5p and fibroblast growth factor 2 (FGF2) in OS tissues and cells were detected using reverse transcription-quantitative polymerase chain reaction. OS cell proliferation, migration and invasion were analysed by MTT, wound healing and Transwell invasion assays, respectively. The targeting relationships between SNHG1 and miR-424-5p, as well as between miR-424-5p and FGF2, were confirmed using RNA-binding protein immunoprecipitation and/or dual-luciferase reporter gene assays. The results demonstrated that the expression levels of SNHG1 and FGF2 were upregulated, whereas the expression of miR-424-5p was downregulated in OS tissues and cells. The silencing of SNHG1 significantly inhibited the proliferation, migration and invasion of OS cells. Additionally, FGF2 was shown to be a target of miR-424-5p, which in turn, was a target of SNHG1. miR-424-5p silencing and FGF2 overexpression both reversed the suppressive effects of SNHG1 knockdown on the proliferation, migration and invasion of OS cells. Thus, the silencing of SNHG1 may inhibit the proliferation, migration and invasion of OS cells by regulating the miR-424-5p/FGF2 axis.

N6-methyladenosine Modification-Related Long Non-Coding RNAs are Potential Biomarkers for Predicting the Prognosis of Patients With Osteosarcoma

“…SNHG1 was upregulated in OS tissues and promoted cell proliferation, invasion, and migration by serving as a ceRNA. 38 – 40 Highly expressed SNHG6 was positively associated with poor overall survival of patients with OS and could enhance OS cell proliferation by regulating the miR-26a-5p/ULK1 axis and expression of p21 and Kruppel-like factor 2 (KLF2). 41 , 42 It has been reported that SNHG7 was aberrantly expressed in OS tissues and elevated levels of SNHG7 could facilitate tumor growth and epithelial-mesenchymal transition (EMT) by regulating p53 expression and miR-34a levels.…”

Osteosarcoma in a ceRNET perspective

“…Nine members of the family have been also reported to drive osteosarcomagenesis through different ceRNETs (Table 1 ). Among them, SNHG1 is consistently reported to be upregulated in OS tissues and cells, correlated with tumor size, TNM stage and lymph node metastasis, predicting poor overall survival [ 162 – 165 ]. In particular, the lncRNA is able to promote proliferation, migration, tumor growth and metastasis, as demonstrated in vitro and in vivo experiments through the ceRNA activity involving the miR-326/NOB1, miR-493/S100A6 and miR-577/Wnt2B axes, with the last one also activating the Wnt/beta-catenin signal pathway, one of the most critical pathway relevant for both cell proliferation and metastasis [ 162 – 164 ].…”

Role of miR-424 in the carcinogenesis

“…For evaluation of their relation to miR-424, following studies have been conducted: In osteosarcoma cell lines Saos-2, MG63, HOS and U2OS, SNHG1 acts as a molecular sponge for miR-424-5p. After knocking down SNHG1, expression levels of miR-424-5p rises and this miRNA can target 3′-UTR of FGF2, resulting in reduced proliferation, migration and invasion [ 16 ]. The same molecular mechanism also applies for cervical cancer cells, but the difference is that sponging molecule is SNHG12 in this case and there is no FGF2 targeting [ 17 ].…”