LncRNA NEAT1: Shedding light on mechanisms and opportunities in liver diseases

With advances in genome and transcriptome research technology, the function and mechanism of lncRNAs in physiological and pathological states have been gradually revealed. Nuclear Enriched Abundant Transcript 1 (NEAT1, a long non‐coding RNA), a vital component of paraspeckles, plays an indispensable...

Full description

Saved in:
Bibliographic Details
Published in:Liver international 2020-11, Vol.40 (11), p.2612-2626
Main Authors: Bu, Fang‐tian, Wang, Ao, Zhu, Yan, You, Hong‐mei, Zhang, Ya‐fei, Meng, Xiao‐ming, Huang, Cheng, Li, Jun
Format: Article
Language:English
Subjects:
Cancer
Carcinoma, Hepatocellular - genetics
Fatty liver
Fibrosis
Gene expression
Genomes
HCC
Hepatocellular carcinoma
Humans
Inflammation
Inflammatory response
Liver
Liver diseases
liver fibrosis
Liver Neoplasms - genetics
lncRNA
NAFLD
NEAT1
Non-alcoholic Fatty Liver Disease - genetics
Non-coding RNA
paraspeckle
Pathogenesis
Regulatory mechanisms (biology)
Ribonucleic acid
RNA
RNA, Long Noncoding - genetics
Transcription
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:With advances in genome and transcriptome research technology, the function and mechanism of lncRNAs in physiological and pathological states have been gradually revealed. Nuclear Enriched Abundant Transcript 1 (NEAT1, a long non‐coding RNA), a vital component of paraspeckles, plays an indispensable role in the formation and integrity of paraspeckles. Throughout the research history, NEAT1 is mostly aberrantly upregulated in various cancers, and high expression of NEAT1 often contributes to poor prognosis of patients. Notably, the role and mechanism of NEAT1 in liver diseases have been increasingly reported. NEAT1 accelerates the progression of non‐alcoholic fatty liver disease (NAFLD), liver fibrosis and hepatocellular carcinoma, while exerting a protective role in the pathogenesis of acute‐on‐chronic liver failure by inhibiting the inflammatory response. In this review, we will elaborate on relevant studies on the different casting of NEAT1 in liver diseases, especially focusing on its regulatory mechanisms and new opportunities for alcoholic liver disease.
ISSN:1478-3223
1478-3231
DOI:10.1111/liv.14629