Entry Detail

General Information

Database ID: LDA0007865
Species: Homo sapiens
Confidence Score: 0.731059
Contents: >> ncRNA Information
>> ncRNA Association Statistics
>> Disease Information
>> Disease Association Statistics
>> Evidence Support
>> Reference
Causality: Yes
Clinical Significance: Unknown

 


ncRNA Information

Reference Genome Note: GRCh38 for human lncRNAs; GRCm39 for mouse lncRNAs; mRatBN7.2 for rat lncRNAs; hg19 for human circRNAs; mm9 for mouse circRNAs.

ncRNA Symbol:NEAT1
Full Name:nuclear paraspeckle assembly transcript 1
Category:LncRNA
Species:Homo sapiens
Synonyms:LINC00084|NCRNA00084|TP53LC15|TncRNA|VINC
Chromosome:11
Strand:+
Coordinate:
Start Site(bp):65422798End Site(bp):65445540
External Links:
Ensembl ID:ENSG00000245532
Ensembl Transcript ID:N/A
Entrez Gene:283131.0
NONCODE ID:N/A
RefSeq Accession:NR_131012.1

 

ncRNA Association Statistics

Total Associated Disease Number:190   
More Information
Causal Disease Number:146
Network:
Top Causal Diseases:
Parkinson Disease  (Score: 1)
Ovarian Neoplasms  (Score: 1)
Non-alcoholic Fatty Liver Disease  (Score: 1)
Parkinson Disease  (Score: 1)
Leukemia, Myeloid, Acute  (Score: 1)
Osteosarcoma  (Score: 1)
Osteosarcoma  (Score: 1)
Leukemia, Myeloid, Acute  (Score: 1)
Colorectal Neoplasms  (Score: 1)
Carcinoma, Hepatocellular  (Score: 1)
More Information

 

 

Disease Information

 Disease OntologyMeSH
Disease ID:D008103
Disease Name:Liver Cirrhosis
Category:MeSH
Type:Digestive System Diseases
Define:Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.
Alias:Liver Cirrhosis//Hepatic Cirrhosis//Cirrhosis, Hepatic//Cirrhosis, Liver//Fibrosis, Liver//Liver Fibrosis

 

Disease Association Statistics

Total Associated ncRNA Number:18   
More Information
Causal ncRNA Number:12
Network:
Top Causal ncRNAs:
lnc-ADD3-AS1  (Score: 0.731059)
CREBBP  (Score: 0.731059)
SCARNA10  (Score: 0.731059)
circFBXW4  (Score: 0.731059)
MBI‑52  (Score: 0.731059)
NEAT1  (Score: 0.731059)
lnc-ADD3-AS1  (Score: 0.731059)
CREBBP  (Score: 0.731059)
SCARNA10  (Score: 0.731059)
circFBXW4  (Score: 0.731059)
More Information

 

Evidence Support

Strong Evidence:In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Migration Assay//Flow Cytometry//FISH//qRT-PCR//RIP//IF//Luciferase Report Assay//Cell Proliferation Assay//IP//IHC//ChIP
Weak Evidence:

 

Reference

[1] PubMed ID:34531378
Disease Name:Liver Cirrhosis
Sample:fibrotic liver tissues
Dysfunction Pattern:Interaction(miR-139-5p/ β-catenin/SOX9/TGF-β1 Pathway)
Validated Method:In Vivo Experiment//RNA Pull-Down//ChIP//Western Blot//Transfection//Migration Assay//Flow Cytometry//FISH//qRT-PCR//RIP//Luciferase Report Assay//Cell Proliferation Assay//IP//IHC//IF
Description:Our results demonstrated that the expression of lncRNA NEAT1 was increased and the expression of miR-139-5p was decreased in fibrotic liver tissues.LncRNA NEAT1 could sponge miR-139-5p and promoted hepatic stellate cells (HSCs) activation by directly inhibiting the expression of miR-139-5p. The co-localization of lncRNA NEAT1 with miR-139-5p was shown in the cytosols of activated HSCs. LncRNA NEAT1 exacerbated liver fibrosis by suppressing the expression of miR-139-5p. Collectively, our study suggested that miR-139-5p sponged by lncRNA NEAT1 regulated liver fibrosis via targeting β-catenin/SOX9/TGF-β1 Pathway.
Causality:Yes
Causal Description:miR-139-5p upregulation could suppress the expression of β-catenin. The overexpression of β-catenin promoted HSCs activation. Moreover, we found that β-catenin could interact with SOX9 promoted HSCs activation. Our further studies demonstrated that SOX9 could bind with the TGF-β1 promoter and promoted the transcription activity of TGF-β1. The upregulation of TGF-β1 further promoted HSCs activation. In vivo study also suggested that lncRNA NEAT1 knockdown and miR-139-5p overexpression alleviated murine liver fibrosis.
Clinical-realted Application: