Retraction Note: 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/s13018-020-02000-1

Cited by 9 publications

(15 citation statements)

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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 [21]. Shen et al reported that lncRNA HOTAIR was highly expressed in osteoporosis patients, which prevented osteogenic differentiation by regulating Wnt/βcatenin pathway [22].…”

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) was 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. Alkaline phosphatase (ALP) activity and Alizarin Red S (ARS) staining were also used to evaluate the osteogenic ability of hBMSCs.Results: The expression levels of LINC00899 were gradually increased, but miR-374a expression was decreased with the prolongation of osteogenic induction. In addition, 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. 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 the osteogenic differentiation of hBMSCs and prevented 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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“…Upregulation of miR-214, miR-363-3p, and miR-142-5p accelerates PI3K/AKT signaling by targeting phosphatase and tensin homolog (PTEN), which is an inhibitor of PI3K [108][109][110][111]. In addition, the excessive expression of lncRNA-TUG1 also gives rise to downregulated PTEN, which may be relevant to the positive effect of TUG1 on osteoclastogenesis [112]. lncRNA-CRNDE also promotes osteoclast proliferation via the PI3K/AKT signaling pathway.…”

Section: Nf-κb and Relatedmentioning

confidence: 99%

Involvement of Noncoding RNAs in the Differentiation of Osteoclasts

Zhao

Jia

Zheng

et al. 2020

Stem Cells International

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As the most important bone-resorbing cells, osteoclasts play fundamental roles in bone remodeling and skeletal health. Much effort has been focused on identifying the regulators of osteoclast metabolism. Noncoding RNAs (ncRNAs) reportedly regulate osteoclast formation, differentiation, survival, and bone-resorbing activity to participate in bone physiology and pathology. The present review intends to provide a general framework for how ncRNAs and their targets regulate osteoclast differentiation and the important events of osteoclastogenesis they are involved in, including osteoclast precursor generation, early differentiation, mononuclear osteoclast fusion, and multinucleated osteoclast function and survival. This framework is beneficial for understanding bone biology and for identifying the potential biomarkers or therapeutic targets of bone diseases. The review also summarizes the results of in vivo experiments and classic experiment methods for osteoclast-related researches.

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“…Skeletal system diseases, including osteoporosis, osteoarthritis, and osteosarcoma, are related to the dysregulation of lncRNAs expression in cartilage and bone cells 9 . For example, lncRNA TUG1 was recently found to be up‐regulated in osteoporosis and regulated osteoclasts proliferation and apoptosis 10 . The lncRNA ORLNC1 could direct MSC fate and thereby regulating bone mass 11 .…”

Section: Introductionmentioning

confidence: 99%

“…9 For example, lncRNA TUG1 was recently found to be upregulated in osteoporosis and regulated osteoclasts proliferation and apoptosis. 10 The lncRNA ORLNC1 could direct MSC fate and thereby regulating bone mass. 11 The expression of lncRNA MSC-AS1 was increased during osteogenic differentiation and played as protective role in steoporosis.…”

Section: Introductionmentioning

confidence: 99%

Iron accumulation regulates osteoblast apoptosis through lncRNAXIST/miR‐758‐3p/caspase 3 axis leading to osteoporosis

Wang

Chen

et al. 2021

IUBMB Life

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Postmenopausal osteoporosis (PMOP) is mainly caused by multiple factors. Recent studies have suggested that iron accumulation (IA) was closely related to PMOP. However, the detailed molecular mechanisms have not been well demonstrated. We constructed the IA mouse model by intraperitoneal injections of ferric ammonium citrate (FAC) and cell model by culturing with the medium containing FAC. Osteoporosis was confirmed in mouse bone tissues using H&E staining, and the level of serum ferritin, alkaline phosphatase (ALP), procollagen-1 N-terminal peptide (P1NP), and osteocalcin in mice was examined by ELISA. The expressions of XIST and miR-758-3p were detected by qRT-PCR. Cell proliferation and apoptosis were measured by CCK-8, TUNEL, and flow cytometry. The expression levels of apoptotic-related proteins were evaluated by western blot. Dual luciferase reporter assay was used to examine the molecular interaction. The expressions of ALP, P1NP, and osteocalcin, and the H&E staining of bone tissues in mice were analyzed to confirm the biological function of XIST and miR-758-3p in vivo. XIST was up-regulated while miR-758-3p was down-regulated in IA mouse and cell models. XIST knockdown significantly reduced FAC-induced osteoblast apoptosis, which was mimicked by transfection with miR-758-3p mimics. XIST acted as a sponge of miR-758-3p, which targeted caspase 3. IA led to the high expression of XIST and promoted osteoblast apoptosis through miR-758-3p/caspase 3. Transfection with shXIST or miR-758-3p mimics alleviated IA-induced mouse osteoporosis. IA regulated osteoblast apoptosis through XIST/miR-758-3p/caspase 3 axis, which might provide alternative targets for the treatment of osteoporosis.

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Retraction Note: LncRNA TUG1 was upregulated in osteoporosis and regulates the proliferation and apoptosis of osteoclasts

Abstract: An amendment to this paper has been published and can be accessed via the original article.

Cited by 9 publications

References 1 publication

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

Involvement of Noncoding RNAs in the Differentiation of Osteoclasts

Iron accumulation regulates osteoblast apoptosis through lncRNAXIST/miR‐758‐3p/caspase 3 axis leading to osteoporosis

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