ArticleCancer biology & therapy2022
Interference of EFNA4 suppresses cell proliferation, invasion and angiogenesis in hepatocellular carcinoma by downregulating PYGO2.
Article in Cancer biology & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Development of a four-gene prognostic signature for hepatocellular carcinoma using TCGA and GEO datasets.Discover oncology · 2026Article
- Coordinated Multicellular Immune Programs and Drug Targets Revealed by Single-Cell Analysis in Driver-Mutated NSCLC.International journal of molecular sciences · 2026Article
- Ephrin-A4 ligand promotes gastric cancer cell epithelial-mesenchymal transition via the PI3K/AKT signaling pathway.Discover oncology · 2026Article
- Proteomics mediates the effects of biological aging on the progression of cardio-renal-metabolic comorbidity: a UK biobank cohort study.Cardiovascular diabetology · 2025Article
- EFNA4 deletion suppresses the migration, invasion, stemness, and angiogenesis of gastric cancer cells through the inactivation of Pygo2/Wnt signaling.Histology and histopathology · 2025Article
- PYGO2 promotes resistance to chemotherapy via reducing apoptosis and G2/M cell cycle arrest in esophageal carcinoma cells.Medical oncology (Northwood, London, England) · 2025Article
- Pygo2+ T cells possess immunosuppressive features and inferior immunotherapeutic response in gastric cancer.Frontiers in immunology · 2025Article
- Ephs in cancer progression: complexity and context-dependent nature in signaling, angiogenesis and immunity.Cell communication and signaling : CCS · 2024Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the most common type of liver cancer. Ephrin A4 (EFNA4) acts as an oncogene in multiple cancers but is little known in HCC. It is revealed that EFNA4 is highly expressed in patients with HCC and influences the proliferation of HCC cells; however, detailed regulatory mechanism of EFNA4 in HCC needs to be unveiled. Here, we discovered that EFNA4 was highly expressed in HCC cell lines. EFNA4 knockdown greatly suppressed cell proliferation, migration and invasion, as well as inhibiting angiogenesis in Huh7 cells. EFNA4 was demonstrated to interact with pygopus-2 (PYGO2) and positively regulate PYGO2 expression. Gene gain- and loss-of-function experiments revealed that the anti-tumor effect of EFNA4 knockdown was partly abolished by PYGO2 overexpression. Furthermore, EFNA4 knockdown blocked wnt/β-catenin signaling in Huh7 cells, which was then abolished by PYGO2. In conclusion, this study further ensured the oncogenic role of EFNA4 in HCC, and disclosed that EFNA4 knockdown suppressed cell proliferation, invasion, angiogenesis, and wnt/β-catenin signaling in HCC by downregulating PYGO2.
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