ArticleGenes & genomics2023
ETV4 facilitates proliferation, migration, and invasion of liver cancer by mediating TGF-β signal transduction through activation of B3GNT3.
Article in Genes & genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Machine Learning-Driven PCDI Classifier for Invasive PitNETs.Current gene therapy · 2026Article
- Article
- Emerging role of ETV4 in colorectal cancer: from molecular mechanisms to clinical implications.Frontiers in oncology · 2026Review
- Article
- ETV4/ALYREF-mediated glycolytic metabolism through PKM2 enhances resistance to ferroptosis and promotes the development of intrahepatic cholangiocarcinoma.Cancer & metabolism · 2025Article
- Identification of ETV4 as a prognostic biomarker and correlates with immune cell infiltration in head and neck squamous cell carcinoma.Scientific reports · 2025Article
- Biological effect of ETV4 and the underlying mechanism of its regulatory effect on epithelial‑mesenchymal transition in intrahepatic cholangiocarcinoma cells.Oncology letters · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMetastasis of liver cancer (LC) is the main cause of its high mortality. ETV4 is a critical regulatory factor in promoting LC progression, but the mechanism that ETV4 impacts LC proliferation, migration, and invasion is poorly understood.
objectiveInvestigation of the molecular mechanism of LC metastasis is conducive to developing effective drugs that prevent LC metastasis.
methodsExpression of ETV4 and its target gene B3GNT3 in LC tissue was analyzed by bioinformatics, and the result was further verified in LC cells by qRT-PCR. In vitro cellular assays evaluated the impact of ETV4 on the proliferation, migration, and invasion of LC cells. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter gene assay were conducted to analyze the interaction between B3GNT3 and ETV4. SB525334 suppressor was used to treat and access the activation of ETV4 on the TGF-β pathway.
resultsWe discovered that ETV4 and B3GNT3 were evidently up-regulated in LC, and high expression of ETV4 was coupled to the increase of proliferation, migration, and invasion of LC cells and epithelial-mesenchymal transition ability. Besides, ETV4 could bind to the B3GNT3 promoter and activate its transcription. Knockdown of B3GNT3 could prominently suppress the effect of up-regulated ETV4 on LC cells. Meanwhile, ETV4 could activate the TGF-β signaling pathway via B3GNT3, while SB525334 treatment notably repressed the functions of ETV4.
conclusionETV4 emerges as a driven oncogene in LC, and the ETV4/B3GNT3-TGF-β pathway promotes proliferation, migration, invasion, and epithelial-mesenchymal transition progress of LC. Inhibition of the pathway may provide an underlying method for the prevention and treatment of LC metastasis.
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