ArticleCell biology and toxicology2023
LncRNA Tug1 relieves the steatosis of SelenoF-knockout hepatocytes via sponging miR-1934-3p.
Article in Cell biology and toxicology, 2023. 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, 10 citations in OpenAlex.
- lncRNAInternational journal of molecular medicine · 2026Article
- LncRNA TUG1 promotes hepatic lipid accumulation by targeting the miR-29a-3p/SREBP-2/HMGCR axis in MAFLD.Functional & integrative genomics · 2026Article
- Dysregulation of the AMPK-SREBP1-FASN axis in MASLD: driving a vicious cycle of lipotoxicity and metabolic-immune crosstalk.Lipids in health and disease · 2026Review
- Overexpression of the lncRNA TUG1 regulates high-glucose-induced endocytic clearance dysfunction in HLSECs via the Wnt/β-catenin signaling pathway.European journal of medical research · 2025Article
- Deciphering the role ofWorld journal of hepatology · 2025Review
- Cadmium Exposure Induces Apoptosis and Necrosis of Thyroid Cells via the Regulation of miR-494-3p/PTEN Axis.Biological trace element research · 2024Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
Metabolic dysfunction associated with fatty liver disease (MAFLD), always accompanied by disturbance of glucose and lipid metabolism, is becoming the most difficult obstacle in the next decades. In the current research, we uncover that the potent non-coding RNA Tug1, which is related to metabolic enzymes, regulates hepatocytes steatosis induced by sodium palmitate via miR-1934-3p absorbing. The knockdown of lncRNA-Tug1 distinctly rescues the increased expression level of glycolytic enzymes and fatty acid synthetase via releasing more mature miR-1934-3p in hepatocytes. Moreover, miR-1934-3p suppresses Selenoprotein F (SelenoF) through binding with the SelenoF 3'UTR effectors; importantly, we demonstrated that the deletion of SelenoF consistent with the lncRNA-Tug1's effecting on metabolism enzymes. In the current paper, the interaction of Tug1/miR-1934-3p/SelenoF was verified by the dual-luciferase reporter system, and IRS1/AKT pathway possesses the essential role in glucolipid metabolism when SelenoF is deleted. We concluded that lncRNA Tug1 functioned as ceRNA to alleviate steatosis and glycolysis in hepatocytes of C57BL/6 through adsorbing miR-1934-3p to release SelenoF and triggering IRS/AKT pathway. The Tug1/miR-1934-3p/SelenoF constructed the ceRNA interact network Selenoprotein F accelerates glucolipid metabolism via IRS1/AKT pathway SelenoF-/- alleviates steatosis in mice liver.
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