ArticleOncotarget2013
EI24 regulates epithelial-to-mesenchymal transition and tumor progression by suppressing TRAF2-mediated NF-κB activity.
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- TRAF6 as a potential target in advanced breast cancer: a systematic review, meta-analysis, and bioinformatics validation.Scientific reports · 2023Pooled it
- Biological significance, molecular mechanisms and clinical potential of EI24 in cancer.Chinese medical journal · 2026Review
- Microbiota-induced EI24 improves homeostasis but impedes function of alveolar macrophages via metabolic regulation.Nature communications · 2026Article
- EI24 suppresses TNBC tumorigenesis by regulating AKT signaling.Frontiers in oncology · 2026Article
- Ei24 deficiency in brown adipocytes induces severe hypothermia under cold stress independent of UCP1 activity.Nature communications · 2025Article
- Inflammation and cancer cell survival: TRAF2 as a key player.Cell death & disease · 2025Review
- Review
- CIGB-300-Regulated Proteome Reveals Common and Tailored Response Patterns of AML Cells to CK2 Inhibition.Frontiers in molecular biosciences · 2022Article
- Circular RNA hsa_circ_0043278 inhibits breast cancer progression via the miR-455-3p/EI24 signalling pathway.BMC cancer · 2021Article
- In search for biomarkers and potential drug targets for uterine serous endometrial cancer.Journal of cancer research and clinical oncology · 2021Article
- Dissecting pharmacological effects of chloroquine in cancer treatment: interference with inflammatory signaling pathways.Immunology · 2020Review
- EI24 Inhibits Cell Proliferation and Drug Resistance of Esophageal Squamous Cell Carcinoma.Frontiers in oncology · 2020Article
- The central regulator p62 between ubiquitin proteasome system and autophagy and its role in the mitophagy and Parkinson's disease.BMB reports · 2020Review
- EI24, as a Component of Autophagy, Is Involved in Pancreatic Cell Proliferation.Frontiers in oncology · 2019Article
- DNA damage triggers tubular endoplasmic reticulum extension to promote apoptosis by facilitating ER-mitochondria signaling.Cell research · 2018Article
- Emerging Paradigm of Crosstalk between Autophagy and the Ubiquitin-Proteasome System.Molecules and cells · 2017Review
- MicroRNA-455-3p promotes invasion and migration in triple negative breast cancer by targeting tumor suppressor EI24.Oncotarget · 2017Article
- Functional characterization of EI24-induced autophagy in the degradation of RING-domain E3 ligases.Autophagy · 2016Article
- Sur8/Shoc2 promotes cell motility and metastasis through activation of Ras-PI3K signaling.Oncotarget · 2015Article
- Curcumin restores sensitivity to retinoic acid in triple negative breast cancer cells.BMC cancer · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor metastasis is a multistep process that requires the concerted activity of discrete biological functions. The epithelial-to-mesenchymal transition (EMT) is the most critical mechanism implicated in tumor progression that is controlled by the inflammatory microenvironment. Understanding how an inflammatory microenvironment is maintained and contributes to tumor progression will be crucial for the development of new effective therapies. Here, we report that etoposide induced 2.4 (EI24) has a multifaceted role against tumor progression that is regulated by both EMT and inflammation. Decreased expression levels of EI24 in epithelial tumor cells induced EMT in association with increased cell motility and invasiveness and resistance to anoikis. Overexpression of EI24 resulted in the opposite cell biological characteristics and suppressed in vivometastatic behavior. EI24 attenuated NF-κB activity by binding to the Complex I component TRAF2 and inducing its lysosome-dependent degradation, leading to transcriptional alterations of EMT- and inflammation-related genes. Analysis of clinical samples demonstrated that reduced EI24 expression and copy number was positively correlated with tumor malignancy and poor prognosis. Collectively, these findings establish EI24 as a critical suppressor of tumor progression and implicate EI24 expression level in malignant tumors as a useful therapeutic and diagnostic marker.
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Registered trials
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.