NEAT1 accelerates the progression of liver fibrosis via regulation of microRNA-122 and Kruppel-like factor 6

Yu, Fang; Jiang, Zhe; Chen, Bicheng; Dong, Peihong; Zheng, Jianjian

doi:10.1007/s00109-017-1586-5

Cited by 80 publications

(77 citation statements)

References 44 publications

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“…NEAT1 showed highly variable expression levels in the SN, which may reflect its reaction to a wide variety of stimuli, including estrogen (25), hepatic fibrosis (59), oxidative stress, and treatment with various therapeutics including simvastatin and fenofibrate (this study)—possibly through the effects of these drugs on the activity of transcription factors of the PPAR family (60, 61), binding sites for which and for their interactor retinoid X receptor-α lie upstream to the NEAT1 transcription start site (47, 62). This offers another mechanism to explain the neuroprotective traits of these drugs (16, 60, 63, 64) and calls for investigating the effects of additional blood-brain barrier–penetrable agents on NEAT1 levels.…”

Section: Discussionmentioning

confidence: 99%

NEAT1 is overexpressed in Parkinson's disease substantia nigra and confers drug‐inducible neuroprotection from oxidative stress

et al. 2019

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Recent reports attribute numerous regulatory functions to the nuclear paraspeckle‐forming long non‐coding RNA, nuclear enriched assembly transcript 1 (NEAT1), but the implications of its involvement in Parkinson's disease (PD) remain controversial. To address this issue, we assessed NEAT1 expression levels and cell type patterns in the substantia nigra (SN) from 53 donors with and without PD, as well as in interference tissue culture tests followed by multiple in‐house and web‐available models of PD. PCR quantification identified elevated levels of NEAT1 expression in the PD SN compared with control brains, an elevation that was reproducible across a multitude of disease models. In situ RNA hybridization supported neuron‐specific formation of NEATl‐based para‐speckles at the SN and demonstrated coincreases of NEAT1 and paraspeckles in cultured cells under paraquat (PQ)‐induced oxidative stress. Furthermore, neuroprotective agents, including fenofibrate and simvastatin, induced NEAT1 up‐regulation, whereas RNA interference—mediated depletion of NEAT1 exacerbated death of PQ‐exposed cells in a leucine‐rich repeat kinase 2‐mediated manner. Our findings highlight a novel protective role for NEAT1 in PD and suggest a previously unknown mechanism for the neuroprotective traits of widely used preventive therapeutics.—Simchovitz, A., Hanan, M., Niederhoffer, N., Madrer, N., Yayon, N., Bennett, E. R., Greenberg, D. S., Kadener, S., Soreq, H. NEAT1 is overexpressed in Parkinson's disease substantia nigra and confers drug‐inducible neuroprotection from oxidative stress. FASEB J. 33, 11223–11234 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

NEAT1 is overexpressed in Parkinson's disease substantia nigra and confers drug‐inducible neuroprotection from oxidative stress

et al. 2019

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“…Nuclear-enriched abundant transcript 1 (NEAT1) is located in 11q13 [128]. The expression of NEAT1 was found to be increased in primary HSCs derived from CCl4-treated mice compared to control mice [74]. NEAT1 overexpression promoted the activation of HSCs and increased levels of Actα2 and Col1α1, indicating that this lncRNA plays a role in HSC activation [36].…”

Section: Neat1mentioning

confidence: 99%

“…NEAT1 overexpression promoted the activation of HSCs and increased levels of Actα2 and Col1α1, indicating that this lncRNA plays a role in HSC activation [36]. NEAT1 overexpression corresponded with decreased levels of miR-122, which was identified to regulate NEAT1 effects on the activation of HSCs by a mechanism associated with Kruppel-like factor 6 (Klf6) [36,74]. The expression of NEAT1 was up-regulated in HCC, while its knockdown was correlated with decreases not only in HCC cell proliferation, but with also invasion, and migration via regulating heterogeneous nuclear ribonucleoprotein A2 (hnRNP A2) [75].…”

Section: Neat1mentioning

confidence: 99%

LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma

Kim

Park

Lee

2020

IJMS

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Long non-coding RNAs (lncRNAs) are emerging as important contributors to the biological processes underlying the pathophysiology of various human diseases, including hepatocellular carcinoma (HCC). However, the involvement of these molecules in chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD) and viral hepatitis, has only recently been considered in scientific research. While extensive studies on the pathogenesis of the development of HCC from hepatic fibrosis have been conducted, their regulatory molecular mechanisms are still only partially understood. The underlying mechanisms related to lncRNAs leading to HCC from chronic liver diseases and cirrhosis have not yet been entirely elucidated. Therefore, elucidating the functional roles of lncRNAs in chronic liver disease and HCC can contribute to a better understanding of the molecular mechanisms, and may help in developing novel diagnostic biomarkers and therapeutic targets for HCC, as well as in preventing the progression of chronic liver disease to HCC. Here, we comprehensively review and briefly summarize some lncRNAs that participate in both hepatic fibrosis and HCC.

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“…In addition, NEAT1 also played an important regulatory role in some diseases, such as acute kidney injury [14], neuropathic pain [15] and liver fibrosis [16]. Previous study has shown that NEAT1 was overexpressed in AAA [17]; nevertheless, the function and mechanism of NEAT1 in AAA remain obscure.…”

Section: Introductionmentioning

confidence: 99%

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

et al. 2020

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Long noncoding RNAs (lncRNAs) were viewed as crucial participants in the pathogenesis of abdominal aortic aneurysm (AAA). LncRNA NEAT1 was recognized as an oncogenic gene in various diseases. However, its function and mechanism in AAA were not precisely documented. Here, we explored the functional role and molecular mechanism of NEAT1 in AAA. Functionally, the effect of NEAT1 on the proliferation was assessed by CCK-8 and EdU assay, while its impact on the apoptosis was evaluated through caspase-3/9 activity and TUNEL assays. As a result, we found that NEAT1 knockdown enhanced the proliferation and impaired the apoptosis of vascular smooth muscle cells (VSMCs). Reversely, overexpressed NEAT1 exerted anti-proliferation and pro-apoptosis effects in VSMCs. Mechanically, we found that STAT3 acted as a transcription factor and contributed to NEAT1 transcription by ChIP and luciferase reporter assays. In addition, NEAT1 was confirmed as a sponge of miR-4688 and thereby increase the expression of TULP3 in VSMCs via RIP assay and RNA pull-down assay. Rescue experiments indicted that TULP3 overexpressing countervailed the impact of NEAT1 depletion on AAA biological processes. Conclusively, lncRNA NEAT1 induced by STAT3 was identified as a ceRNA and facilitated AAA formation by targeting miR-4688/TULP3 axis.

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NEAT1 accelerates the progression of liver fibrosis via regulation of microRNA-122 and Kruppel-like factor 6

Cited by 80 publications

References 44 publications

NEAT1 is overexpressed in Parkinson's disease substantia nigra and confers drug‐inducible neuroprotection from oxidative stress

NEAT1 is overexpressed in Parkinson's disease substantia nigra and confers drug‐inducible neuroprotection from oxidative stress

LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

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