ArticleDiscover oncology2025
LncRNA EBLN3P/microRNA-323a-3p/EphA1 axis affects the biological function of hepatocellular carcinoma cells.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Circular RNA hsa_circ_0001829 promotes pancreatic ductal adenocarcinoma through miR-7113-3p/DTX4 axis.World journal of surgical oncology · 2026Article
- ScRNA-Seq Deciphers an Autocrine EFNA1-EPHA1 Loop That Reprograms the Microenvironment in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Article
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Authors and funding
8 authors.
Funding
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Abstract
objectiveThis study focused on the capabilities of lncRNA endogenous bornavirus-like nucleoprotein 3, pseudogene (EBLN3P) and microRNA-323a-3p (miR-323a-3p) on hepatocellular carcinoma (HCC) cells activities via EPH receptor A1 (EphA1).
methodsExpression levels of EBLN3P, miR-323a-3p, and EphA1 were evaluated in HCC tissues and cells. Subsequently, we further analyzed the link between EBLN3P expression and HCC clinicopathological features. The binding sites of EBLN3P and miR-323a-3p, as well as miR-323a-3p and EphA1, were verified via various molecular assays. HCC cell activities were assessed by CCK-8 assay, Transwell assay and flow cytometry, respectively. An in vivo subcutaneous tumor inhibition model was performed to validate tumor growth.
resultsIn EBLN3P-silenced HCC cells, there was a notable decrease in cell proliferation, invasive, and migratory capabilities, accompanied by an enhanced apoptosis rate. EBLN3P could competitively bind miR-323a-3p to downregulate miR-323a-3p. Overexpression of miR-323a-3p neutralized the oncogenic role of EBLN3P on HCC cell activities. miR-323a-3p directly targeted EphA1. Overexpression of EphA1 counteracted the suppressive role of miR-323a-3p on HCC cell activities. In vivo experiments demonstrated that downregulation of EBLN3P inhibited tumor growththrough the miR-323a-3p/EphA1 axis.
conclusionEBLN3P promotes HCC development by regulating the miR-323a-3p/EphA1 axis. Interfering with EBLN3P effectively restrains proliferation, migration, and invasion of HCC cells by upregulating miR-323a-3p and downregulating EphA1. This mechanism provides new molecular evidence for HCC pathogenesis, suggesting EBLN3P as a potential target in HCC treatment. Future research should explore the interaction between this axis and other tumor-related signaling pathways to support the development of targeted therapeutic strategies.
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