ArticleJournal of biochemistry2021
ETV4 mediates the Wnt/β-catenin pathway through transcriptional activation of ANXA2 to promote hepatitis B virus-associated liver hepatocellular carcinoma progression.
Article in Journal of biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Emerging role of ETV4 in colorectal cancer: from molecular mechanisms to clinical implications.Frontiers in oncology · 2026Review
- ANXA2 in hepatocellular carcinoma: orchestrating tumorigenesis, progression, and therapeutic resistance toward precision targeting.Journal of translational medicine · 2025Review
- EP300 Modulates MCM8 Transcription and Augments the Malignant Phenotype of Hepatitis B Virus-Positive Hepatocellular Carcinoma Cells.The Kaohsiung journal of medical sciences · 2025Article
- FadA antigen of Fusobacterium nucleatum: implications for ceRNA network in colorectal cancer and adenomatous polyps progression.Discover oncology · 2025Article
- Role of the Annexin A protein family in liver diseases: insights and therapeutic opportunities.Frontiers in pharmacology · 2025Review
- ETV4 interacts with LOXL2 to induce epigenetic activation of NID1 during colorectal cancer progression.International journal of biological sciences · 2025Article
- The pathogenic germline ETV4 P433L mutation identified in multiple primary lung cancer affect tumor stem-like property by Wnt/β-catenin pathway.Cell death & disease · 2024Article
- LCN2 Promotes Proliferation and Glycolysis by Activating the JAK2/STAT3 Signaling Pathway in Hepatocellular Carcinoma.Applied biochemistry and biotechnology · 2024Article
- Wnt/β-Catenin signaling pathway in hepatocellular carcinoma: pathogenic role and therapeutic target.Frontiers in oncology · 2024Review
- E74-like ETS transcription factor 1 promotes the progression of pancreatic cancer by regulating doublecortin-like kinase 1/Janus kinase/signal transducer and activator of transcription pathway.American journal of cancer research · 2024Article
- Review
- ETV4 facilitates proliferation, migration, and invasion of liver cancer by mediating TGF-β signal transduction through activation of B3GNT3.Genes & genomics · 2023Article
- Infectious Agents Induce Wnt/β-Catenin Pathway Deregulation in Primary Liver Cancers.Microorganisms · 2023Review
- Annexin A protein family: Focusing on the occurrence, progression and treatment of cancer.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
- Erratum issuedErratum.2022
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ETS variant 4 (ETV4) has been implicated in the development of various cancers. However, the molecular events mediated by ETV4 in liver cancer are poorly understood, especially in hepatitis B virus (HBV)-associated liver hepatocellular carcinoma (LIHC). Here, we aimed to identify the target involved in ETV4-driven hepatocarcinogenesis. Bioinformatics analysis revealed that ETV4 was highly expressed in patients with HBV-associated LIHC, and HBV infection promoted the expression of ETV4 in LIHC cells. Inhibition of ETV4 repressed the proliferation, migration, invasion of LIHC cells and suppressed the secretion of HBV and the replication of HBV DNA. ANXA2 expression in LIHC patients was positively correlated with ETV4 expression. Chromatin immunoprecipitation and dual-luciferase reporter assays revealed that ETV4 elevated the ANXA2 expression at the transcriptional level by binding to the ANXA2 promoter. Overexpression of ANXA2 reversed the inhibitory effect of sh-ETV4 on the malignant biological behaviours of HBV-infected LIHC cells by activating the Wnt/β-catenin pathway. In conclusion, ETV4 mediates the activation of Wnt/β-catenin pathway through transcriptional activation of ANXA2 expression to promote HBV-associated LIHC progression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.