Abstract
BackgroundLong non-coding RNA (LncRNA) TUG1 plays critical roles in thedevelopment of human cancers. Its inhibition has been proved to participate inankylosing spondylitis, which is an inverse pathological procedure ofosteoporosis. In the present study, we aim to investigate the role of lncRNATUG1 in ankylosing spondylitis.Materials and methodsExpressions of lncRNA TUG1 in plasma of 98 patients withosteoporosis and 60 healthy participants were detected by real-time quantitativePCR (RT-qPCR). Diagnostic values of lncRNA CASC11 for osteoclasts were performedby the ROC curve with osteoporosis patients as positive and healthy participantsas negative. All experiments were repeated 3 times. Mean ± standard deviationwas calculated.ResultsWe found that plasma lncRNA TUG1 was upregulated in osteoporosispatients than in healthy participants. Upregulation of plasma lncRNA TUG1distinguished osteoporosis patients from healthy participants. LncRNA TUG1 levelincreased with the advances of clinical stages. Over-expression of lncRNA TUG1promoted the proliferation and inhibited the apoptosis of mice osteoclasts,while lncRNA TUG1 siRNA silencing played an opposite role. In addition, lncRNATUG1 over-expression led to downregulated PTEN, while lncRNA TUG1 siRNAsilencing played an opposite role.ConclusionTherefore, lncRNA TUG1 is upregulated in osteoporosis and regulatesthe proliferation and apoptosis of osteoclasts. lncRNA TUG1 knockdown may serveas a promising therapeutic target for osteoporosis by inhibiting theproliferation and promoting the apoptosis of osteoclasts through PTEN.
Highlights
R osteoclasts were performed by the receiver operating characteristic (ROC) curve with osteoporosis patients as positive and healthy participants as negative
D addition, Long non-coding RNAs (lncRNAs) taurine upregulated gene 1 (TUG1) over-expression led to downregulated Phosphatase and tensin homolog (PTEN), while lncRNA TUG1 siRNA silencing played an opposite role
E Conclusion: lncRNA TUG1 is upregulated in osteoporosis and regulates the proliferation and apoptosis of osteoclasts. lncRNA TUG1 knockdown may serve as a promising therapeutic target for osteoporosis by inhibiting the proliferation and promoting the apoptosis of osteoclasts through PTEN
Summary
R osteoclasts were performed by the ROC curve with osteoporosis patients as positive and healthy participants as negative. Upregulation of plasma lncRNA TUG1 distinguished osteoporosis patients from healthy participants. LncRNA TUG1 level increased with the advances of clinical stages. Over-expression of lncRNA TUG1 promoted the proliferation and inhibited the apoptosis of mice osteoclasts, while lncRNA TUG1 siRNA silencing played an opposite role. In. D addition, lncRNA TUG1 over-expression led to downregulated PTEN, while lncRNA TUG1 siRNA silencing played an opposite role. LncRNA TUG1 is upregulated in osteoporosis and regulates the proliferation and apoptosis of osteoclasts. LncRNA TUG1 knockdown may serve as a promising therapeutic target for osteoporosis by inhibiting the proliferation and promoting the apoptosis of osteoclasts through PTEN. The incidence rate of osteoporosis is higher in women than
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