ArticleMolecular and cellular biochemistry2020
LncRNA KCNQ1OT1 ameliorates the liver injury induced by acetaminophen through the regulation of miR-122-5p/CES2 axis.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Diet intervention altered DNA methylation of potassium voltage-gated channel subfamily Q member 1 in metabolic dysfunction-associated steatohepatitis.Clinical epigenetics · 2026Article
- Deletion of miR-122-5p Exacerbated Hyperthyroidism-Induced Liver Injury by Regulating Ferroptosis.International journal of endocrinology · 2026Article
- LncRNA SNHG7 Knockdown Aggravates Hepatic Ischemia-Reperfusion Injury and Promotes Apoptosis in Hemorrhagic Shock Pregnant Rats by Modulating miR-34a-5p/YWHAG Axis.Molecular biotechnology · 2023Article
- A human liver organoid screening platform for DILI risk prediction.Journal of hepatology · 2023Article
- Potential of long non-coding RNA KCNQ1OT1 as a biomarker reflecting systemic inflammation, multiple organ dysfunction, and mortality risk in sepsis patients.Journal of clinical laboratory analysis · 2021Article
- Role of Noncoding RNAs in Acetaminophen-Induced Liver Injury.Gene expression · 2021Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs (lncRNAs) have been shown to be implicated in acetaminophen (APAP)-induced liver injury (AILI). We applied this study to investigate the role and functional mechanism of KCNQ1 overlapping transcript 1 (KCNQ1OT1) in AILI. The AILI model was established by APAP treatment in mice. The liver injury was preliminarily evaluated by ALT and AST activities via the detection kits. The quantitative real-time polymerase chain reaction (qRT-PCR) was exploited for detecting the expression of KCNQ1OT1, microRNA-122-5p (miR-122-5p), and carboxylesterase 2 (CES2). Protein levels were analyzed via Western blot. 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) assay, and flow cytometry were separately applied to determine cell proliferation and apoptosis rate. Inflammation was assessed by enzyme-linked immunosorbent assay (ELISA). Dual-luciferase reporter assay was implemented to testify the intergenic combination. The function of KCNQ1OT1 in vivo was explored through KCNQ1OT1 knockdown in mice. APAP triggered the downregulation of KCNQ1OT1 and CES2 in mice serums. KCNQ1OT1 upregulation could relieve the AILI in HepaRG cells, which were abrogated by CES2 downregulation. KCNQ1OT1 served as a sponge of miR-122-5p and miR-122-5p directly targeted CES2. KCNQ1OT1 overexpression abated the AILI through the miR-122-5p/CES2 axis in HepaRG cells in vitro and mice in vivo. The collective results clarified that KCNQ1OT1 weakened the AILI in vitro and in vivo by the miR-122-5p/CES2 axis, providing an explicit molecular mechanism and selectable therapeutic strategy of AILI.
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