Faculty Opinions recommendation of The H19 long noncoding RNA is a novel negative regulator of cardiomyocyte hypertrophy.

2018 ◽  
Author(s):  
Timothy McKinsey
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Negative Regulator ◽  
Cardiomyocyte Hypertrophy

scholarly journals GW29-e1174 The H19 long noncoding RNA is a novel negative regulator of cardiomyocyte hypertrophy

2018 ◽  
Vol 72 (16) ◽  
pp. C36
Author(s):  
Lantao Liu ◽  
Yao Song ◽  
Linling Li ◽  
Song Zuo ◽  
Nian Liu ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Negative Regulator ◽  
Cardiomyocyte Hypertrophy

scholarly journals The H19 long noncoding RNA is a novel negative regulator of cardiomyocyte hypertrophy

2016 ◽  
Vol 111 (1) ◽  
pp. 56-65 ◽  
Author(s):  
Lantao Liu ◽  
Xiangbo An ◽  
Zhenhua Li ◽  
Yao Song ◽  
Linling Li ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Negative Regulator ◽  
Cardiomyocyte Hypertrophy

scholarly journals Long Noncoding RNA NRAV Promotes Respiratory Syncytial Virus Replication by Targeting the MicroRNA miR-509-3p/Rab5c Axis To Regulate Vesicle Transportation

2020 ◽  
Vol 94 (10) ◽  
Author(s):  
Jian Li ◽  
Miao Li ◽  
Xiuli Wang ◽  
Mengfei Sun ◽  
Cuiqing Ma ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Respiratory Virus ◽  
Antiviral Response ◽  
Negative Regulator ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Tract Infections

ABSTRACT Respiratory syncytial virus (RSV) is an enveloped RNA virus which is responsible for approximately 80% of lower respiratory tract infections in children. Current lines of evidence have supported the functional involvement of long noncoding RNA (lncRNA) in many viral infectious diseases. However, the overall biological effect and clinical role of lncRNAs in RSV infection remain unclear. In this study, lncRNAs related to respiratory virus infection were obtained from the lncRNA database, and we collected 144 clinical sputum specimens to identify lncRNAs related to RSV infection. Quantitative PCR (qPCR) detection indicated that the expression of lncRNA negative regulator of antiviral response (NRAV) in RSV-positive patients was significantly lower than that in uninfected patients, but lncRNA psoriasis-associated non-protein coding RNA induced by stress (PRINS), nuclear paraspeckle assembly transcript 1 (NEAT1), and Nettoie Salmonella pas Theiler’s (NeST) showed no difference in vivo and in vitro. Meanwhile, overexpression of NRAV promoted RSV proliferation in A549 and BEAS-2B cells, and vice versa, indicating that the downregulation of NRAV was part of the host antiviral defense. RNA fluorescent in situ hybridization (FISH) confirmed that NRAV was mainly located in the cytoplasm. Through RNA sequencing, we found that Rab5c, which is a vesicle transporting protein, showed the same change trend as NRAV. Subsequent investigation revealed that NRAV was able to favor RSV production indirectly by sponging microRNA miR-509-3p so as to release Rab5c and facilitate vesicle transportation. The study provides a new insight into virus-host interaction through noncoding RNA, which may contribute to exploring potential antivirus targets for respiratory virus. IMPORTANCE The mechanism of interaction between RSV and host noncoding RNAs is not fully understood. In this study, we found that the expression of long noncoding RNA (lncRNA) negative regulator of antiviral response (NRAV) was reduced in RSV-infected patients, and overexpression of NRAV facilitated RSV production in vitro, suggesting that the reduction of NRAV in RSV infection was part of the host antiviral response. We also found that NRAV competed with vesicle protein Rab5c for microRNA miR509-3p in cytoplasm to promote RSV vesicle transport and accelerate RSV proliferation, thereby improving our understanding of the pathogenic mechanism of RSV infection.

scholarly journals Flicr, a long noncoding RNA, modulates Foxp3 expression and autoimmunity

2017 ◽  
Vol 114 (17) ◽  
pp. E3472-E3480 ◽  
Author(s):  
David Zemmour ◽  
Alvin Pratama ◽  
Scott M. Loughhead ◽  
Diane Mathis ◽  
Christophe Benoist
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Autoimmune Diabetes ◽  
Foxp3 Expression ◽  
Chromatin Accessibility ◽  
Negative Regulator ◽  
Additional Layer ◽  
Accessible Region ◽  
Long Intergenic Noncoding Rna ◽  
The Impact

A combination of transcription factors, enhancers, and epigenetic marks determines the expression of the key transcription factor FoxP3 in regulatory T cells (Tregs). Adding an additional layer of complexity, the long noncoding RNA (lncRNA) Flicr (Foxp3 long intergenic noncoding RNA) is a negative regulator that tunes Foxp3 expression, resulting in a subset of Tregs with twofold- to fivefold-lower levels of FoxP3 protein. The impact of Flicr is particularly marked in conditions of IL-2 deficiency, and, conversely, IL-2 represses Flicr expression. Flicr neighbors Foxp3 in mouse and human genomes, is specifically expressed in mature Tregs, and acts only in cis. It does not affect DNA methylation, but modifies chromatin accessibility in the conserved noncoding sequence 3 (CNS3)/Accessible region 5 (AR5) region of Foxp3. Like many lncRNAs, Flicr’s molecular effects are subtle, but by curtailing Treg activity, Flicr markedly promotes autoimmune diabetes and, conversely, restrains antiviral responses. This mechanism of FoxP3 control may allow escape from dominant Treg control during infection or cancer, at the cost of heightened autoimmunity.

The long noncoding RNA XIST protects cardiomyocyte hypertrophy by targeting miR-330-3p

2018 ◽  
Vol 505 (3) ◽  
pp. 807-815 ◽  
Author(s):  
Yuewu Chen ◽  
Xianxia Liu ◽  
Lei Chen ◽  
Weiwei Chen ◽  
Yuansheng Zhang ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cardiomyocyte Hypertrophy

scholarly journals Long Noncoding RNA NTT Context-Dependently Regulates MYB by Interacting With Activated Complex in Hepatocellular Carcinoma Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Ya-Sian Chang ◽  
Ya-Ting Lee ◽  
Ju-Chen Yen ◽  
Yuli C. Chang ◽  
Li-Li Lin ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Target Genes ◽  
Metabolic Diseases ◽  
Cellular Migration ◽  
Negative Regulator ◽  
Dependent Manner ◽  
Colon Cancers ◽  
Activated Complex

BackgroundLong noncoding RNA (lncRNA) mediates the pathogenesis of various diseases, including cancer and cardiovascular, infectious, and metabolic diseases. This study examined the role of lncRNA NTT in the development and progression of cancer.MethodsThe expression of NTT was determined using tissues containing complementary DNA (cDNA) from patients with liver, lung, kidney, oral, and colon cancers. The expression of cis-acting genes adjacent to the NTT locus (CTGF, STX7, MYB, BCLAF1, IFNGR1, TNFAIP3, and HIVEP2) was also assessed. We used knockdown and chromatin immunoprecipitation (ChIP) assays to identify the cis-acting genes that interact with NTT.ResultsNTT was most significantly downregulated in hepatocellular carcinoma (HCC), while a higher NTT level correlated with a shorter survival time of patients with HCC. Multivariate analysis indicated NTT was not an independent predictor for overall survival. MYB was significantly upregulated, and its increased expression was associated with dismal survival in HCC patients, similar to the results for NTT. NTT knockdown significantly decreased cellular migration. ChIP of HCC cell lines revealed that NTT is regulated by the transcription factor ATF3 and binds to the MYB promoter via the activated complex. Additionally, when NTT was knocked down, the expression of MYB target genes such as Bcl-xL, cyclinD1, and VEGF was also downregulated. NTT could play a positive or negative regulator for MYB with a context-dependent manner in both HCC tissues and animal model.ConclusionOur study suggests that NTT plays a key role in HCC progression via MYB-regulated target genes and may serve as a novel therapeutic target.

scholarly journals NF-κB-Interacting Long Noncoding RNA Regulates HIV-1 Replication and Latency by Repressing NF-κB Signaling

2020 ◽  
Vol 94 (17) ◽  
Author(s):  
Hong Wang ◽  
Yue Liu ◽  
Chen Huan ◽  
Jing Yang ◽  
Zhaolong Li ◽  
...  
Keyword(s):  
Long Terminal Repeat ◽  
Long Noncoding Rna ◽  
Transcription Initiation ◽  
Noncoding Rna ◽  
Ectopic Expression ◽  
Terminal Repeat ◽  
Negative Regulator ◽  
Dependent Manner ◽  
Iκb Kinase ◽  
Hiv 1

ABSTRACT NF-κB-interacting long noncoding RNA (NKILA) was recently identified as a negative regulator of NF-κB signaling and plays an important role in the development of various cancers. It is well known that NF-κB-mediated activation of human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR)-driven gene expression is required for HIV-1 transcription and reactivation of latency. However, whether NKILA plays essential roles in HIV-1 replication and latency is unclear. Here, by ectopic expression and silencing experiments, we demonstrate that NKILA potently inhibits HIV-1 replication in an NF-κB-dependent manner by suppressing HIV-1 LTR promoter activity. Moreover, NKILA showed broad-spectrum inhibition on the replication of HIV-1 clones with different coreceptor tropisms as well as on LTR activity of various HIV-1 clinical subtypes. Chromatin immunoprecipitation (ChIP) assays revealed that NKILA expression abolishes the recruitment of p65 to the duplicated κB binding sites in the HIV-1 LTR. NKILA mutants disrupting NF-κB inhibition also lost the ability to inhibit HIV-1 replication. Notably, HIV-1 infection or reactivation significantly downregulated NKILA expression in T cells in order to facilitate viral replication. Downregulated NKILA was mainly due to reduced acetylation of histone K27 on the promoter of NKILA by HIV-1 infection, which blocks NKILA expression. Knockdown of NKILA promoted the reactivation of latent HIV-1 upon phorbol myristate acetate (PMA) stimulation, while ectopic NKILA suppressed the reactivation in a well-established clinical model of withdrawal of azidothymidine (AZT) in vitro. These findings improve our understanding of the functional suppression of HIV-1 replication and latency by NKILA through NF-κB signaling. IMPORTANCE The NF-κB pathway plays key roles in HIV-1 replication and reactivation of HIV-1 latency. A regulator inhibiting NF-κB activation may be a promising therapeutic strategy against HIV-1. Recently, NF-κB-interacting long noncoding RNA (NKILA) was identified to suppress the development of different human cancers by inhibiting IκB kinase (IKK)-induced IκB phosphorylation and NF-κB pathway activation, whereas the relationship between NKILA and HIV-1 replication is still unknown. Here, our results show that NKILA inhibits HIV-1 replication and reactivation by suppressing HIV-1 long terminal repeat (LTR)-driven transcription initiation. Moreover, NKILA inhibited the replication of HIV-1 clones with different coreceptor tropisms. This project may reveal a target for the development of novel anti-HIV drugs.

scholarly journals HDAC2 Inhibits EMT-Mediated Cancer Metastasis by Downregulating the Long Noncoding RNA H19 in Colorectal Cancer

2020 ◽  
Author(s):  
Xue-ting Hu ◽  
Wei Xing ◽  
Rong-sen Zhao ◽  
Yan Tan ◽  
Xiao-feng Wu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cancer Metastasis ◽  
Rna Binding ◽  
Underlying Mechanism ◽  
Negative Regulator ◽  
Clinical Prognosis ◽  
Mesenchymal Transition ◽  
Injection Model

Abstract Background: Epithelial to mesenchymal transition (EMT) is a critical step for cancer metastasis, which is regulated by epigenetic mechanisms. The role of HDACs-mediated deacytelation remains unclear in colorectal cancer (CRC) metastasis. Here, we revealed the biological role and underlying mechanism of histone deacetylase2 (HDAC2) in EMT-mediated CRC metastasis. Methods: The expression of HDACs in CRC was analyzed using the public database Oncomine and TCGA, human colorectal tumor primary sites and paired metastatic tissues, high or low metastatic CRC cell lines (DLD1, HCT116, SW480 and SW620). Microarray analysis was used to detect the gene expression changes in HDAC2 knock out CRC cells. Epithelial-mesenchymal transition (EMT)-related proteins were determined using western blot and immunofluorescence. CRC cell metastasis was assessed by transwell assay. To study the underlying mechanism of HDAC2 in EMT-mediated CRC metastasis, we performed chromatin immunoprecipitation, promoter activity, co-immunoprecipitation and RNA-binding protein immunoprecipitation assays through using CRC cells and specific siRNAs targeting H19, SP1 and MMP14. Finally, CRC metastasis in vivo was performed using a tail vain injection model. Results: Our data showed that the expression of HDAC2 was reduced in CRC metastatic tissues and and low HDAC2 expression predicted a poor clinical prognosis in CRC patients. HDAC2 deletion or knock down in CRC cells induced EMT and metastasis by upregulating the long noncoding RNA H19 (LncRNA H19). HDAC2 decreased histone H3K27 acetylation at the promoter of LncRNA H19 and its expression via a SP1-dependent mechanism. LncRNA H19 functioned as a miR-22-3P sponge to increase the expression of MMP14. Finally, using a tail vain injection model, we showed the HDAC2 loss strongly induces lung metastasis, which is suppressed by LncRNA H19 knockdown. Conclusion: Our study proved that HDAC2 is a negative regulator of EMT-mediated CRC metastasis through regulating H19 and MMP14 expression.

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