Up-regulated HOTAIR induced by fatty acids inhibits PTEN expression and increases triglycerides accumulation in HepG2 cells

Li, Weiping; Chen, Xiaoge; Lin, Miaozhi; Huang, Dongyang

doi:10.1080/16546628.2017.1412794

Cited by 9 publications

(6 citation statements)

References 36 publications

(60 reference statements)

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“…steatosis), while the ‘second hit’ is the progression of steatosis to nonalcoholic steatohepatitis (NASH) ( 8 ). This progression is often associated with the release of cytokines, and a previous study identified a central role for the overexpression of pro-inflammatory cytokine tumour necrosis factor (TNF)-α mRNA in the aetiology of NASH ( 9 ). Human liver steatosis is associated with the accumulation of excess oleic acid (OA), a monosaturated omega-9 fatty acid and end product of de novo fatty acid synthesis ( 10 ).…”

Section: Popular Scientific Summarymentioning

confidence: 99%

Bile salt hydrolase-overexpressing Lactobacillus strains can improve hepatic lipid accumulation in vitro in an NAFLD cell model

Huang

Wang

Xia

et al. 2020

Food & Nutrition Research

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Background Non-alcoholic fatty liver disease (NAFLD) includes a range of liver diseases that occur in the absence of significant alcohol consumption. The probiotic bacterial strains Lactobacillus casei LC2W, which overexpresses the bile salt hydrolase (BSH) gene (referred to as pWQH01), and Lactobacillus plantarum AR113, which exhibits high BSH activity, have been shown to improve hepatic lipid accumulation and may lower cholesterol levels in vivo . These effects may be BSH-dependent, as L. casei LC2W without BSH activity did not exert these beneficial effects. Objective This study aimed to investigate the effects of Lactobacillus with high BSH activity on cholesterol accumulation and lipid metabolism abnormalities in oleic acid (OA)- and cholesterol-induced HepG2 cell models, and to determine the mechanism underlying the effects. Design A HepG2 cell model of OA-induced steatosis and cholesterol-induced cholesterol accumulation was developed. OA- and cholesterol-treated HepG2 cells were incubated with L. plantarum AR113, L. casei LC2W or L. casei pWQH01 for 6 h at 37°C with 5% CO 2 . Subsequently, a series of indicators and gene expressions were analysed. Results Both L. plantarum AR113 and L. casei pWQH01 significantly reduced lipid accumulation, total cholesterol (TC) levels and 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR) mRNA expression relative to the control group, whereas L. casei LC2W had no similar effect. Additionally, exposure to L. plantarum AR113 or L. casei pWQH01 significantly reduced the expression of sterol regulatory element-binding protein 1c (SREBP-1c), Acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS) and tumour necrosis factor-α (TNF-α) andsignificantly increased the expression of 5' adenosine monophosphate-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor alpha (PPARα). Conclusion Both L. plantarum AR113 and L. casei pWQH01 appear to improve steatosis in vitro in a BSH-dependent manner.

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Section: Popular Scientific Summarymentioning

confidence: 99%

Bile salt hydrolase-overexpressing Lactobacillus strains can improve hepatic lipid accumulation in vitro in an NAFLD cell model

Huang

Wang

Xia

et al. 2020

Food & Nutrition Research

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“…HOTAIR is increased in different forms of cancers and involved in diverse cellular functions. In NAFLD, free fatty acid treatment promotes TG accumulation in HepG2 cells, significantly induces HOTAIR expression and inhibits phosphatase and tensin homolog expression[ 139 ]. A recent study reported that HOTAIR was activated in NAFLD, and HOTAIR knockdown significantly inhibited the development of NAFLD via mediation of miR-130b-3p/ROCK1/AMPK axis, further suggesting a target for NAFLD[ 140 ].…”

Section: Emerging Role Of Ncrnas In the Pathogenesis Of Nafldmentioning

confidence: 99%

Noncoding RNAs as additional mediators of epigenetic regulation in nonalcoholic fatty liver disease

Zaiou¹

2022

WJG

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Nonalcoholic fatty liver disease (NAFLD) has emerged as the most common cause of chronic liver disorder worldwide. It represents a spectrum that includes a continuum of different clinical entities ranging from simple steatosis to nonalcoholic steatohepatitis, which can evolve to cirrhosis and in some cases to hepatocellular carcinoma, ultimately leading to liver failure. The pathogenesis of NAFLD and the mechanisms underlying its progression to more pathological stages are not completely understood. Besides genetic factors, evidence indicates that epigenetic mechanisms occurring in response to environmental stimuli also contribute to the disease risk. Noncoding RNAs (ncRNAs), including microRNAs, long noncoding RNAs, and circular RNAs, are one of the epigenetic factors that play key regulatory roles in the development of NAFLD. As the field of ncRNAs is rapidly evolving, the present review aims to explore the current state of knowledge on the roles of these RNA species in the pathogenesis of NAFLD, highlight relevant mechanisms by which some ncRNAs can modulate regulatory networks implicated in NAFLD, and discuss key challenges and future directions facing current research in the hopes of developing ncRNAs as next-generation non-invasive diagnostics and therapies in NAFLD and subsequent progression to hepatocellular carcinoma.

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“…NEAT1 expression aggravated free fatty acid (FFA)-induced lipid accumulation in hepatocytes by regulating the c-Jun/SREBP1c axis by sponging miR-139-5p. Indeed, NEAT1 heightening is followed by acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) mRNA enhancement in both in vivo and in vitro models of NAFLD [111] . A preclinical study showed that the knockdown of NEAT1 in hepatocytes hampered lipid content and liver disease through the modulation of ACC and FAS expression.…”

Section: Nuclear Enriched Abundant Transcript 1 (Neat1)mentioning

confidence: 99%

Old-fashioned and newly discovered biomarkers: the future of NAFLD-related HCC screening and monitoring

Piciotti¹,

Longo²,

Agresta³

et al. 2022

Hepatoma Res

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Nonalcoholic fatty liver disease (NAFLD) is the major contributor to the global burden of chronic liver diseases and ranges from simple and reversible steatosis to nonalcoholic steatohepatitis (NASH), which may progress into cirrhosis and hepatocellular carcinoma (HCC). HCC represents the most common liver cancer, and it is a leading cause of death worldwide with an increasing trend for the future. Due to late diagnosis, non-responsiveness to systemic therapy, and high cancer heterogeneity, the treatment of this malignancy is challenging. To date, liver biopsy and ultrasound (US) are the gold standard procedures for HCC diagnosis and surveillance, although they are not suitable for mass screening. Therefore, it is impelling to find new, less invasive diagnostic strategies able to detect HCC at an early stage as well as monitor tumor progression and recurrence. Common and rare inherited variations that boost the switching from NASH to liver cancer may help to predict tumor onset. Furthermore, epigenetic changes which reflect intertumoral heterogeneity occur early in tumorigenesis and are highly stable under pathologic conditions. The severity of hepatic injuries can be detected through the analysis of cell circulating tumor DNAs (ctDNAs), microRNAs (miRNAs), and noncoding RNAs (ncRNAs), which are involved in several pathological processes that feature cancer, including cell growth, survival, and differentiation, thus representing appealing biomarkers for HCC. Therefore, this review discusses the current options for HCC surveillance, focusing on the role of genetic and epigenetic biomarkers as new strategies to refine HCC management.

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Up-regulated HOTAIR induced by fatty acids inhibits PTEN expression and increases triglycerides accumulation in HepG2 cells

Cited by 9 publications

References 36 publications

Bile salt hydrolase-overexpressing Lactobacillus strains can improve hepatic lipid accumulation in vitro in an NAFLD cell model

Bile salt hydrolase-overexpressing Lactobacillus strains can improve hepatic lipid accumulation in vitro in an NAFLD cell model

Noncoding RNAs as additional mediators of epigenetic regulation in nonalcoholic fatty liver disease

Old-fashioned and newly discovered biomarkers: the future of NAFLD-related HCC screening and monitoring

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