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

Table 2 Relevant dysregulated long noncoding RNAs associated with alterations in liver metabolism and nonalcoholic fatty liver disease

lncRNA	Expression	Main functional and pathophysiological effects	Ref.
MALAT1	↑	Promotes cell proliferation, migration, and invasion in several different human cancers including HCC	[119-122]
		Promotes hepatic steatosis and insulin resistance
		Hepatic MALAT1 levels are higher in NASH patients with fibrosis
		Promotes NAFLD progression and increase with the severity of the disease
NEAT1	↑	Promotes adipogenesis, lipogenesis, and lipid absorption	[124,126,127]
		Modulates fibrosis and inflammatory responses
		Silencing NEAT1 alleviated fibrosis and inflammatory in a NAFLD cellular model
MEG3	↓	Involved in lipid metabolism and glucose homeostasis	[131-134]
		Correlates with steatosis and inflammation (NASH) in patients with NAFLD
HULC	↑	Promotes HCC growth and metastasis	[135,136]
		Promotes NAFLD development
		Metformin decreases HULC expression
HOTAIR	↑	Activates lipid accumulation in hepatocytes and promotes hepatic steatosis development	[139-141]
		Expression profile is significantly increased in oleic acid-induced steatosis and during the development of HFD-induced NAFLD
		Accelerates liver fibrosis and carcinogenesis
FLRL2	↓	Decreases endoplasmic reticulum stress and liver inflammation	[143]
		Alleviates NAFLD and steatosis in mouse model

FLR2: Fatty liver-related lncRNA 2; H19: H19 imprinted maternally expressed transcript; HCC: Hepatocellular carcinoma; HFD: High-fat diet; HOTAIR: HOX transcript antisense RNA; MALAT1: Metastasis-associated lung adenocarcinoma transcript 1; lncRNAs: Long noncoding RNAs; MEG3: Maternally expressed 3; NAFLD: Nonalcoholic fatty liver disease; NASH: Nonalcoholic steatohepatitis; NEAT1: Nuclear paraspeckle assembly transcript 1; HULC: Hepatocellular carcinoma upregulated long noncoding RNA.