LncRNA HOTAIR accelerates free fatty acid-induced inflammatory response in HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA

LncRNA HOTAIR has been reported to be associated with metabolic diseases of the liver. However, the effect of HOTAIR on non-alcoholic fatty liver disease (NAFLD) inflammation and its potential mechanism have not been reported. Genes and proteins expression were detected by qRT-PCR and Western blot r...

Full description

Saved in:
Bibliographic Details
Published in:Cytotechnology (Dordrecht) 2024-04, Vol.76 (2), p.259-269
Main Authors: Guo, Bo, Yan, Shengzhe, Zhai, Lei, Cheng, Yanzhen
Format: Article
Language:English
Subjects:
Biochemistry
Biomedicine
Biotechnology
Cell culture
Cell viability
Chemistry
Chemistry and Materials Science
Enzyme-linked immunosorbent assay
Fatty acids
Fatty liver
Glucose
Inflammation
Lipids
Liver cancer
Liver diseases
Metabolic disorders
Metabolism
mRNA stability
Non-coding RNA
Oxidative stress
Pathogenesis
Proteins
Reagents
Software
Splicing factors
Statistical analysis
Transcription factors
Variance analysis
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:LncRNA HOTAIR has been reported to be associated with metabolic diseases of the liver. However, the effect of HOTAIR on non-alcoholic fatty liver disease (NAFLD) inflammation and its potential mechanism have not been reported. Genes and proteins expression were detected by qRT-PCR and Western blot respectively. The level of inflammatory cytokines was assessed by ELISA. HepG2 cell viability was detected by MTT assay. TG level and lipid accumulation were measured by Assay Kit and Oil red O staining, respectively. Direct binding relationship between HOTAIR and Serine/arginine splicing factor 1 (SRSF1), SRSF1 and MLX interacting protein like (MLXIPL) were confirmed by RNA-pull down and RIP assay. HOTAIR was highly expressed in free fatty acids (FFA)-treated HepG2 cells. HOTAIR knockdown alleviated FFA-induced inflammation of HepG2 cells. Then further analysis showed that HOTAIR and SRSF1 had a mutual binding relationship, and HOTAIR maintained MLXIPL mRNA stability via recruiting SRSF1 in HepG2 cells. Moreover, the inhibitory effect of HOTAIR knockdown on FFA-induced inflammation in HepG2 cells was reversed by MLXIPL overexpression. HOTAIR accelerates inflammation of FFA-induced HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA, which will help to find new effective strategies for NAFLD therapy.
ISSN:0920-9069
1573-0778
DOI:10.1007/s10616-023-00614-x