LncRNA TUG1 sponges miR-204-5p to promote osteoblast differentiation through upregulating Runx2 in aortic valve calcification

Cong, Yu; Li, Lifu; Xie, Fei; Guo, Shichao; Liu, Fa-Yuan; Dong, Nianguo; Wang, Yongjun

doi:10.1093/cvr/cvx180

Cited by 213 publications

(143 citation statements)

References 49 publications

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“…Accumulated studies have demonstrated a significant role for long noncoding RNAs (lncRNAs) in regulating gene expression, including a significant influence on biological activities in the skeletal system, such as in osteoporosis and osteoarthritis . For example, lncRNA TUG1 promoted the differentiation of osteoblast by sponging miR‐204‐5p, which led to the up‐regulation of Runx2 . LncRNA MEG3 restrained the osteogenic differentiation of BMSCs by targeting miR‐133a‐3p .…”

Section: Introductionmentioning

confidence: 99%

“…7 For example, lncRNA TUG1 promoted the differentiation of osteoblast by sponging miR-204-5p, which led to the up-regulation of Runx2. 8 LncRNA MEG3 restrained the osteogenic differentiation of BMSCs by targeting miR-133a-3p. 9 Some studies also revealed that lncRNAs acted as epigenetic regulators in the osteo-adipogenic lineage commitment because of the reciprocal relationship between osteogenic and adipogenic differentiation.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA‐PCAT1 targeting miR‐145‐5p promotes TLR4‐associated osteogenic differentiation of adipose‐derived stem cells

et al. 2018

J Cellular Molecular Medi

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This study was aimed to explore the differential expression of long noncoding RNAs (lncRNA)‐PCAT1, miR‐145‐5p and TLR4 in osteogenic differentiation via the Toll‐like receptor (TLR) signalling pathway and consequently determine the potential molecular mechanism. The mRNAs and pathways related to the osteogenic differentiation in human adipose‐derived stem cells (hADSCs) were analysed by bioinformatics. The MiRanda and TargetScan database were employed to detect the potential binding sites of miRNAs on lncRNAs and mRNAs. The differential expression of lncRNA‐PCAT1, miR‐145‐5p and TLR4 were detected by qRT‐PCR. Rrelated protein expression was analysed by Western blot. The targeted relationships between lncRNA‐PCAT1, miR‐145‐5p and TLR4 were verified by dual‐luciferase reporter assay. Alkaline phosphatase (ALP) activity and ARS staining assays were used to measure the impacts exerted by lncRNA PCAT1, miR‐145‐5p and TLR4 mRNA on osteogenic differentiation. After the induction of osteoblast differentiation, the expression of lncRNA‐PCAT1 and TLR4 increased, while the expression of miR‐145‐5p decreased. Dual‐luciferase reporter assay confirmed the targeted relationship between lncRNA‐PCAT1, miR‐145‐5p, and TLR4. LncRNA‐PCAT1 negatively regulated miR‐145‐5p and positively regulated TLR4. Knockdown of lncRNA‐PCAT1 or TLR4 decreased the expression of osteogenic differentiation‐related proteins, reduced the ALP and ARS levels and the activity of the TLR signalling pathway. MiR‐145‐5p could reverse the effects of PCAT1 and TLR4 in hADSCs osteogenic differentiation. LncRNA‐PCAT1 negatively regulated miR‐145‐5p, which promoted TLR4 expression to promote osteogenic differentiation by activating the TLR signalling pathway.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

LncRNA‐PCAT1 targeting miR‐145‐5p promotes TLR4‐associated osteogenic differentiation of adipose‐derived stem cells

et al. 2018

J Cellular Molecular Medi

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“…TUG1 has been reported to play critical roles in the progression of many human diseases, such as cancer, aortic valve calcification and pre-eclampsia. [8][9][10] Indeed, TUG1 can regulate gene expression via diverse mechanisms during various biological processes, including inflammatory response. Overexpression of TUG1 has been shown to protect the mouse liver against cold-induced injury by inhibiting apoptosis and inflammation, 11 whereas TUG1 knockdown inhibits hyperlipidaemia, decreases inflammatory response and alleviates atherosclerotic lesions.…”

mentioning

confidence: 99%

Long non‐coding RNA TUG1 promotes airway remodelling by suppressing the miR‐145‐5p/DUSP6 axis in cigarette smoke‐induced COPD

Yuan

Wang

et al. 2019

J Cellular Molecular Medi

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Chronic obstructive pulmonary disease (COPD) is a progressive lung disease that is primarily caused by cigarette smoke (CS)‐induced chronic inflammation. In this study, we investigated the function and mechanism of action of the long non‐coding RNA (lncRNA) taurine‐up‐regulated gene 1 (TUG1) in CS‐induced COPD. We found that the expression of TUG1 was significantly higher in the sputum cells and lung tissues of patients with COPD as compared to that in non‐smokers, and negatively correlated with the percentage of predicted forced expiratory volume in 1 second. In addition, up‐regulation of TUG1 was observed in CS‐exposed mice, and knockdown of TUG1 attenuated inflammation and airway remodelling in a mouse model. Moreover, TUG1 expression was higher in CS extract (CSE)‐treated human bronchial epithelial cells and lung fibroblasts, whereas inhibition of TUG1 reversed CSE‐induced inflammation and collagen deposition in vitro. Mechanistically, TUG1 promoted the expression of dual‐specificity phosphatase 6 (DUSP6) by sponging miR‐145‐5p. DUSP6 overexpression reversed TUG1 knockdown‐mediated inhibition of inflammation and airway remodelling. These findings suggested an important role of TUG1 in the pathological alterations associated with CS‐mediated airway remodelling in COPD. Thus, TUG1 may be a promising therapeutic target in CS‐induced airway inflammation and fibroblast activation.

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“…Bioinformatics algorithm found that miR-204-5p was a target gene of LOC285758. miR-204 was previously reported to be involved in a series of physiological and pathological processes, such as diabetic retinopathy, aortic valve disease and ulcerative disease [25][26][27]. Some recent studies revealed that miR-204-5p also exerts antitumor effects on various cancers (e.g., breast cancer, melanoma and liver cancer) through inhibiting invasion and metastasis of cancer cells [25,[28][29][30].…”

Section: Discussionmentioning

confidence: 99%

The long non‐coding RNA LOC285758 promotes invasion of acute myeloid leukemia cells by down‐regulating miR‐204‐5p

Xue

Che

2020

FEBS Open Bio

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Acute myeloid leukemia (AML) is the second most common type of leukemia worldwide. It was previously reported that expression of the long noncoding RNA LOC285758 is positively associated with AML cell proliferation, but the underlying mechanisms have not previously been reported. Here, we report that LOC285758 expression is higher in clinical AML blood samples and cultured AML cells. miR‐204‐5p was confirmed to be a target gene of LOC285758 by bioinformatics analysis and luciferase assay. LOC285758 overexpression promoted AML cell viability and invasion abilities, which were effectively inhibited by miR‐204‐5p overexpression; moreover, miR‐204‐5p overexpression also regulated the expression of E‐cadherin, N‐cadherin and Twist1. The data also showed that increased LOC285758 expression could effectively suppress the earlier effects of miR‐204‐5p on AML cells. Our findings suggest that targeting of miR‐204‐5p by LOC285758 promotes the cell viability and invasion of AML cells, and thus LOC285758 may have potential as a therapeutic target for AML treatment.

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LncRNA TUG1 sponges miR-204-5p to promote osteoblast differentiation through upregulating Runx2 in aortic valve calcification

Abstract: All together, the evidence generated by our study elucidates the role of lncRNA TUG1 as a miRNA sponge in CAVD, and sheds new light on lncRNA-directed diagnostics and therapeutics in CAVD.

Cited by 213 publications

References 49 publications

LncRNA‐PCAT1 targeting miR‐145‐5p promotes TLR4‐associated osteogenic differentiation of adipose‐derived stem cells

LncRNA‐PCAT1 targeting miR‐145‐5p promotes TLR4‐associated osteogenic differentiation of adipose‐derived stem cells

Long non‐coding RNA TUG1 promotes airway remodelling by suppressing the miR‐145‐5p/DUSP6 axis in cigarette smoke‐induced COPD

The long non‐coding RNA LOC285758 promotes invasion of acute myeloid leukemia cells by down‐regulating miR‐204‐5p

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