LncRNA-ATB/microRNA-200a/β-catenin regulatory axis involved in the progression of HCV-related hepatic fibrosis

Fu, Na; Zhao, Suxian; Kong, Lingbo; Du, Jinghua; Ren, Wei-Guang; Han, Fang; Zhang, Qingshan; Li, Wencong; Cui, Po; Wang, Rongqi; Zhang, Yuguo; Nan, Yuemin

doi:10.1016/j.gene.2017.03.008

Cited by 52 publications

(36 citation statements)

References 28 publications

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“…miRNAs are differentially expressed during the course of liver fibrosis. For instance, the increased expression of miR‐125a and miR‐34a as well as the decreased expression of miR‐181, miR‐200a, and miR‐29b are observed in fibrotic livers . miR‐150 is reduced in activated HSCs and its mimics decreases HSC activation through inhibiting c‐myb expression .…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA HOTTIP mediates SRF expression through sponging miR‐150 in hepatic stellate cells

Zheng

Mao

Dong

et al. 2018

J Cellular Molecular Medi

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HOXA transcript at the distal tip (HOTTIP) has been shown to be up‐regulated in a variety of cancers and is identified as an oncogenic long noncoding RNA. However, the biological role of HOTTIP in liver fibrosis is unclear. Here, we reported that HOTTIP was specifically overexpressed in activated hepatic stellate cells (HSCs). HOTTIP knockdown suppressed the activation and proliferation of HSCs. Luciferase reporter assay showed that HOTTIP and serum response factor (SRF) were targets of miR‐150. RNA binding protein immunoprecipitation assay indicated the interaction between miR‐150 and HOTTIP. Further study revealed that HOTTIP increased SRF expression as a competing endogenous RNA for miR‐150, thus prompting HSC activation. Taken together, we provide a novel HOTTIP‐miR‐150‐SRF signalling cascade in liver fibrosis.

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Section: Introductionmentioning

confidence: 99%

Long noncoding RNA HOTTIP mediates SRF expression through sponging miR‐150 in hepatic stellate cells

Zheng

Mao

Dong

et al. 2018

J Cellular Molecular Medi

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“…In this study, downregulated lncRNA-ATB expression levels dysregulated endogenous miR-200a and then reduced β-catenin expression to suppress LX-2 cell activation [64]. Thus, the lncRNA-ATB/miR-200a/β-catenin regulatory axis likely plays important roles in the progression of liver fibrosis in hepatitis C virus (HCV) patients [64]. This suggests that lncRNA-ATB knockdown might be a potential therapeutic target for HCV-related liver fibrosis.…”

Section: Lncrna-atbmentioning

confidence: 82%

“…LncRNA activated by transforming growth factor beta (LncRNA-ATB) has been reported to be related to hepatocellular carcinoma invasion by regulating miR-200a target genes [89]. In another viral liver disease model, lncRNA-ATB was upregulated in hepatitis C virus-related fibrotic liver tissues and included the common binding sites for β-catenin and miR-200a [64]. In this study, downregulated lncRNA-ATB expression levels dysregulated endogenous miR-200a and then reduced β-catenin expression to suppress LX-2 cell activation [64].…”

Section: Lncrna-atbmentioning

confidence: 99%

“…In another viral liver disease model, lncRNA-ATB was upregulated in hepatitis C virus-related fibrotic liver tissues and included the common binding sites for β-catenin and miR-200a [64]. In this study, downregulated lncRNA-ATB expression levels dysregulated endogenous miR-200a and then reduced β-catenin expression to suppress LX-2 cell activation [64]. Thus, the lncRNA-ATB/miR-200a/β-catenin regulatory axis likely plays important roles in the progression of liver fibrosis in hepatitis C virus (HCV) patients [64].…”

Section: Lncrna-atbmentioning

confidence: 99%

“…On the other hand, the Wnt signalling pathway plays important roles in liver fibrosis. LincRNA-p21 [56] and ATB [64] can competitively combine with miRNA to change the protein expression level of β-catenin.…”

Section: Signalling Pathways Involved In Liver Fibrosismentioning

confidence: 99%

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The Roles and Mechanisms of lncRNAs in Liver Fibrosis

Yang

Fan

et al. 2020

IJMS

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Many studies have revealed that circulating long noncoding RNAs (lncRNAs) regulate gene and protein expression in the process of hepatic fibrosis. Liver fibrosis is a reversible wound healing response followed by excessive extracellular matrix accumulation. In the development of liver fibrosis, some lncRNAs regulate diverse cellular processes by acting as competing endogenous RNAs (ceRNAs) and binding proteins. Previous investigations demonstrated that overexpression of lncRNAs such as H19, maternally expressed gene 3 (MEG3), growth arrest-specific transcript 5 (GAS5), Gm5091, NR_002155.1, and HIF 1alpha-antisense RNA 1 (HIF1A-AS1) can inhibit the progression of liver fibrosis. Furthermore, the upregulation of several lncRNAs [e.g., nuclear paraspeckle assembly transcript 1 (NEAT1), hox transcript antisense RNA (Hotair), and liver-enriched fibrosis-associated lncRNA1 (lnc-LFAR1)] has been reported to promote liver fibrosis. This review will focus on the functions and mechanisms of lncRNAs, the lncRNA transcriptome profile of liver fibrosis, and the main lncRNAs involved in the signalling pathways that regulate hepatic fibrosis. This review provides insight into the screening of therapeutic and diagnostic markers of liver fibrosis.

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Long noncoding RNA myocardial infarction–associated transcript regulated the pancreatic stellate cell activation to promote the fibrosis process of chronic pancreatitis

Líu

et al. 2018

J of Cellular Biochemistry

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Background: Long noncoding RNAs (lncRNAs) play crucial roles in fibrosis process. In our previous RNA-seq study, we found that lncRNA myocardial infarction-associated transcript (MIAT) was differentially expressed in pancreatic tissues of chronic pancreatitis (CP) patients. However, the function of MIAT in CP remains unknown. This study was aimed to investigate the function and underlying mechanism of MIAT in pancreatic fibrosis. Materials and Methods: The expression levels of MIAT, miR-216a-3p, cyclooxygenase 2 (COX-2), α-smooth muscle actin (α-SMA), and collagen I were estimated by Western blot analysis and qualitative reverse transcription polymerase chain reaction. The relationships between miR-216a-3p, MIAT, and COX-2 were confirmed by luciferase reporter assay. The proliferation of human pancreatic stellate cells (HPaSteCs) was detected by cell counting kit-8 assay.Results: We found that MIAT, along with the levels of fibrosis-related proteins α-SMA and collagen I, as well as COX-2 were upregulated, while miR-216a-3p was downregulated in transforming growth factor (TGF)-β1-stimulated HPaS-teCs. Mechanistically, MIAT acted as a molecular sponge for miR-216a-3p. Furthermore, we identified COX-2 as a direct target of miR-126a-3p. Additionally, MIAT overturned the inhibitory effect of miR-216a-3p overexpression and COX-2 knockdown on the activation and proliferation of HPaSteCs. Conclusion: Our study provided mechanistic insights into a critical role for MIAT as a miRNA sponge in CP. K E Y W O R D S chronic pancreatitis, human pancreatic stellate cells, long noncoding RNA, myocardial infarction-associated transcript J Cell Biochem. 2019;120:9547-9555.wileyonlinelibrary.com/journal/jcb noncoding RNA myocardial infarction-associated transcript regulated the pancreatic stellate cell activation to promote the fibrosis process of chronic pancreatitis. J Cell Biochem. 2019;120:9547-9555.

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LncRNA-ATB/microRNA-200a/β-catenin regulatory axis involved in the progression of HCV-related hepatic fibrosis

Cited by 52 publications

References 28 publications

Long noncoding RNA HOTTIP mediates SRF expression through sponging miR‐150 in hepatic stellate cells

Long noncoding RNA HOTTIP mediates SRF expression through sponging miR‐150 in hepatic stellate cells

The Roles and Mechanisms of lncRNAs in Liver Fibrosis

Long noncoding RNA myocardial infarction–associated transcript regulated the pancreatic stellate cell activation to promote the fibrosis process of chronic pancreatitis

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