ArticleDigestive diseases and sciences2016
Knockdown of Astrocyte Elevated Gene-1 Inhibits Activation of Hepatic Stellate Cells.
Article in Digestive diseases and sciences, 2016. 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.
- Molecular Pathophysiology of Hepatocellular Carcinoma: From Metabolic Inflammation to Therapeutic Targets.Cancers · 2026Review
- Review
- T4 reduces cisplatin resistance by inhibiting AEG-1 gene expression in lung cancer cells.Scientific reports · 2022Article
- Locostatin Alleviates Liver Fibrosis Induced by Carbon Tetrachloride in Mice.Digestive diseases and sciences · 2019Article
- Hypoxia-inducible factor 1a induces phenotype switch of human aortic vascular smooth muscle cell through PI3K/AKT/AEG-1 signaling.Oncotarget · 2017Article
- Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells.American journal of translational research · 2017Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAstrocyte elevated gene-1 (AEG-1) is a positive regulator of tumorigenesis and a valuable prognostic marker of a diverse array of cancers, including liver cancer; however, the relationship between AEG-1 and hepatic fibrogenesis is not known.
objectiveThe objective of this study was to explore the expression of AEG-1 during hepatic fibrogenesis and determine how AEG-1 regulates the profibrogenic phenotype of hepatic stellate cells (HSCs).
methodsThe levels of AEG-1 were monitored in the fibrotic livers and transforming growth factor-β (TGF-β)- or lipopolysaccharide (LPS)-stimulated HSCs. The expression of AEG-1 was knocked down by lentivirus-mediated short hairpin RNA in HSCs, and collagen expression, proliferation assays, apoptosis induction studies, and migration assays were simultaneously conducted in vitro.
resultsAEG-1 expression was increased in the fibrotic livers. At the cellular level, TGF-β or LPS stimulation, which caused HSC activation, induced AEG-1 expression in HSC-T6 and primary rat HSCs (P < 0.05). Knockdown of AEG-1 inhibited collagen I and α-smooth muscle actin expression (P < 0.05), reduced cell proliferation (P < 0.05) and motility (P < 0.05), and induced cell apoptosis (P < 0.05) in HSCs. This antifibrotic effect caused by lack of AEG-1 was associated with the inactivation of PI3K/Akt and the mitogen-activated protein kinase pathway.
conclusionsKnockdown of AEG-1 suppressed the activation of HSCs by modulating the phenotype and inducing apoptosis. AEG-1 might be a potential target in treatment of hepatic fibrosis.
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