ArticleOncology letters2022
Knockdown of ETV4 promotes autophagy-dependent apoptosis in GBM cells by reducing the transcriptional activation of EMP1.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Epithelial membrane protein 1 in human cancer: a potential diagnostic biomarker and therapeutic target.Biomarkers in medicine · 2024Pooled it
- LncRNA UNC5C-AS1 inhibits angiogenesis and induces endothelial apoptosis via the miR-148a-3p/EMP1 axis in preeclampsia.Cell adhesion & migration · 2026Article
- ETV4 Improves Cerebral Ischemia-Reperfusion Injury by Restraining YBX1-GPX4-Ferroptosis Cascades.Brain and behavior · 2026Article
- HDAC6 inhibition reprograms endothelial and macrophage responses to protect the lung in endotoxemia.Respiratory research · 2026Article
- Emerging role of ETV4 in colorectal cancer: from molecular mechanisms to clinical implications.Frontiers in oncology · 2026Review
- Article
- PEA3 Transcription Factors, Role in Invasion, Proliferation and Radioresistance of Glioblastoma Stem Cells.Journal of cellular and molecular medicine · 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
- The study of an anoikis-related signature to predict glioma prognosis and immune infiltration.Journal of cancer research and clinical oncology · 2023Article
- TAOK3 Facilitates Esophageal Squamous Cell Carcinoma Progression and Cisplatin Resistance Through Augmenting Autophagy Mediated by IRGM.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- Superenhancer activation of KLHDC8A drives glioma ciliation and hedgehog signaling.The Journal of clinical investigation · 2023Article
- Sodium Propionate Contributes to Tumor Cell Growth Inhibition through PPAR-γ Signaling.Cancers · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ETS variant transcription factor 4 (ETV4) is a common cancer-promoting transcription factor and its expression has been found to be significantly upregulated in glioblastoma multiforme (GBM), as determined via analysis of the Gene Expression Profiling Interactive Analysis (GEPIA) database. In addition, our previous study demonstrated that ETV4 expression was highly positively correlated with epithelial membrane protein 1 (EMP1). The present study aimed to determine whether ETV4 could influence the activation of the PI3K/AKT/mTOR signaling pathway to affect the autophagy and apoptosis of GBM cells by regulating the transcriptional activity of EMP1. In addition to the analysis of the GEPIA database, the expression levels of ETV4 were also investigated in several different GBM cell lines. After interfering with the expression of ETV4, western blotting was used to detect the expression levels of autophagy- and apoptosis-related proteins, and a TUNEL assay was used to detect the levels of cell apoptosis. Dual luciferase reporter and chromatin immunoprecipitation assays were used to verify the potential binding site of ETV4 on EMP1. Western blotting was also used to analyze the expression levels of PI3K/AKT/mTOR signaling pathway-related proteins. The results of the current study revealed that the expression levels of ETV4 were significantly upregulated in GBM cell lines compared with those in normal glial cells. In the GBM cell line, LN-229, ETV4 was discovered to bind to the EMP1 promoter and positively regulate the expression of EMP1. The knockdown of ETV4 expression inhibited the PI3K/AKT/mTOR signaling pathway activity to promote autophagy and apoptosis, and this effect could be partially reversed by overexpressing EMP1. In conclusion, these findings indicated that the knockdown of ETV4 in GBM cells may reduce the transcriptional activation of EMP1 and thereby inhibit PI3K/AKT/mTOR signaling pathway activity to promote autophagy and apoptosis. This provides a novel insight into potential strategies for the treatment of GBM via the induction of autophagy-dependent apoptosis.
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