RETRACTED ARTICLE: LncRNA TUG1 was upregulated in osteoporosis
and regulates the proliferation and apoptosis of osteoclasts

Han, Yang; Liu, Chunying; Lei, Ming; Sun, Shaosong; Zheng, Wenjie; Niu, Yanan; Xia, Xi

doi:10.1186/s13018-019-1430-4

Cited by 27 publications

(16 citation statements)

References 23 publications

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“…LncRNA has been con rmed to play a vital role in bone metabolism diseases. Han et al revealed that downregulation of lncRNA TUG1 effectively inhibited osteoclast proliferation and might serve as a potential target for the treatment of osteoporosis [16]. Shen et al reported that lncRNA HOTAIR was highly expressed in osteoporosis patients, which prevented osteogenic differentiation by regulating Wnt/βcatenin pathway [17].…”

Section: Discussionmentioning

confidence: 99%

LINC00899 Promotes Osteogenic Differentiation and Alleviates Osteoporosis via Targeting miR-374a to Regulate RUNX2

Gao

Xue

Yang

2020

Preprint

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Objective: This study aims to illustrate the underlying molecular mechanisms of long noncoding RNAs (LncRNAs) LINC00899 in osteoporosis.Methods: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) used to examine the levels of LINC00899, miR-374a and RUNX2 in clinical tissues or human bone mesenchymal stem cells (hBMSCs). The interaction between miR-374a and LINC00899 or RUNX2 was predicted by starBase and verified by luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay. Results: The expression of LINC00899 was lowly expressed in osteoporotic patients’ bone tissues and knockdown of LINC00899 decreased the expression of osteogenesis-related genes. Moreover, LINC00899 was confirmed to inhibit miR-374a expression by direct interaction. the expression levels of LINC00899 were gradually increased, but miR-374a expression was decreased with the prolongation of osteogenic induction. Finally, we demonstrated that RUNX2 was a target of miR-374a, and the silencing of miR-374a partially abolished the inhibitory effect of LINC00899 knockdown on the expression of RUNX2, OPN and OCN.Conclusions: We demonstrated that LINC00899 facilitated osteogenic differentiation of hBMSCs and prevent osteoporosis by sponging miR-374a and enhancing RUNX2 expression, which might provide a useful therapeutic strategy for osteoporosis patients.

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Section: Discussionmentioning

confidence: 99%

LINC00899 Promotes Osteogenic Differentiation and Alleviates Osteoporosis via Targeting miR-374a to Regulate RUNX2

Gao

Xue

Yang

2020

Preprint

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“…lncRNAs have been shown to regulate osteoclastogenesis by regulating the expression of specific target mRNAs. In osteoporosis, the increased expression of lncRNA TUG1 can regulate the proliferation and apoptosis of osteoclasts through Pten [86]. During the formation of osteoclasts, the expression of lncRNA AK077216 was significantly up-regulated.…”

Section: Lncrna-mediated Mechanismsmentioning

confidence: 99%

The roles of miRNA, lncRNA and circRNA in the development of osteoporosis

et al. 2020

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Osteoporosis is a common metabolic bone disease, influenced by genetic and environmental factors, that increases bone fragility and fracture risk and, therefore, has a serious adverse effect on the quality of life of patients. However, epigenetic mechanisms involved in the development of osteoporosis remain unclear. There is accumulating evidence that epigenetic modifications may represent mechanisms underlying the links of genetic and environmental factors with increased risk of osteoporosis and bone fracture. Some RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), have been shown to be epigenetic regulators with significant involvement in the control of gene expression, affecting multiple biological processes, including bone metabolism. This review summarizes the results of recent studies on the mechanisms of miRNA-, lncRNA-, and circRNA-mediated osteoporosis associated with osteoblasts and osteoclasts. Deeper insights into the roles of these three classes of RNA in osteoporosis could provide unique opportunities for developing novel diagnostic and therapeutic approaches to this disease.

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“…lncRNA TUG1 (taurine-upregulated gene 1) is thought to be upregulated in osteoporosis. This theory is based on the fact that it is inhibited in ankylosing spondylitis, which is commonly thought of as an inverse pathological process to osteoporosis [ 67 ]. In the plasma of patients of both genders at various stages of osteoporosis, there was upregulation of lncRNA TUG1 [ 67 ].…”

Section: The Role Of Micro Rna (Mirna) and Long-non-coding Rna (Lnmentioning

confidence: 99%

“…This theory is based on the fact that it is inhibited in ankylosing spondylitis, which is commonly thought of as an inverse pathological process to osteoporosis [ 67 ]. In the plasma of patients of both genders at various stages of osteoporosis, there was upregulation of lncRNA TUG1 [ 67 ]. Although the mechanism of action of lncRNA TUG1 has not yet been elucidated, it is thought to sponge miR-204-5p to promote osteoblast differentiation [ 67 ].…”

Section: The Role Of Micro Rna (Mirna) and Long-non-coding Rna (Lnmentioning

confidence: 99%

The Role of Micro RNA and Long-Non-Coding RNA in Osteoporosis

Chen

2020

IJMS

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Osteoporosis is a major concern worldwide and can be attributed to an imbalance between osteoblastic bone formation and osteoclastic bone resorption due to the natural aging process. Heritable factors account for 60–80% of optimal bone mineralization; however, the finer details of pathogenesis remain to be elucidated. Micro RNA (miRNA) and long-non-coding RNA (lncRNA) are two targets that have recently come into the spotlight due to their ability to control gene expression at the post-transcriptional level and provide epigenetic modification. miRNAs are a class of non-coding RNAs that are approximately 18–25 nucleotides long. It is thought that up to 60% of human protein-coding genes may be regulated by miRNAs. They have been found to regulate gene expression that controls osteoblast-dependent bone formation and osteoclast-related bone remodeling. lncRNAs are highly structured RNA transcripts longer than 200 nucleotides that do not translate into proteins. They have very complex secondary and tertiary structures and the same degradation processes as messenger RNAs. The fact that they have a rapid turnover is due to their sponge function in binding the miRNAs that lead to a degradation of the lncRNA itself. They can act as signaling, decoy, and framework molecules, or as primers. Current evidence suggests that lncRNAs can act as chromatin and transcriptional as well as post-transcriptional regulators. With regards to osteoporosis, lncRNA is thought to be involved in the proliferation, apoptosis, and inflammatory response of the bone. This review, which is based on a systematic appraisal of the current literature, provides current molecular and genetic opinions on the roles of miRNAs and lncRNAs in osteoporosis. Further research into the epigenetic modification and the regulatory roles of these molecules will bring us closer to potential disease-modifying treatment for osteoporosis. However, more issues regarding the detailed actions of miRNAs and lncRNAs in osteoporosis remain unknown and controversial and warrant future investigation.

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RETRACTED ARTICLE: LncRNA TUG1 was upregulated in osteoporosis and regulates the proliferation and apoptosis of osteoclasts

Cited by 27 publications

References 23 publications

LINC00899 Promotes Osteogenic Differentiation and Alleviates Osteoporosis via Targeting miR-374a to Regulate RUNX2

LINC00899 Promotes Osteogenic Differentiation and Alleviates Osteoporosis via Targeting miR-374a to Regulate RUNX2

The roles of miRNA, lncRNA and circRNA in the development of osteoporosis

The Role of Micro RNA and Long-Non-Coding RNA in Osteoporosis

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