ArticleFrontiers in oncology2020
EI24 Inhibits Cell Proliferation and Drug Resistance of Esophageal Squamous Cell Carcinoma.
Article in Frontiers in oncology, 2020. 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.
- The advancements in organoids: Potential and challenges in researching the esophagus and esophageal squamous cell carcinoma.Genes & diseases · 2026Review
- Biological significance, molecular mechanisms and clinical potential of EI24 in cancer.Chinese medical journal · 2026Review
- EI24 suppresses TNBC tumorigenesis by regulating AKT signaling.Frontiers in oncology · 2026Article
- Single-cell-derived ferroptosis signature predicts prognosis and therapy response in esophageal squamous cell carcinoma.Frontiers in oncology · 2026Article
- Integrative Regulatory Networks of MicroRNA-483: Unveiling Its Systematic Role in Human Diseases and Clinical Implications.Biomolecules · 2025Review
- Long Noncoding RNA Lnc-MTPAP-1 Overexpressed by Particulate Matter Suppresses Apoptosis in Non-Small Cell Lung Cancer (NSCLC) Cells.International journal of molecular sciences · 2025Article
- Genome-wide Cas9-mediated screening of essential non-coding regulatory elements via libraries of paired single-guide RNAs.Nature biomedical engineering · 2024Article
- Review
- Long noncoding RNA HEIH depletion depresses esophageal carcinoma cell progression by upregulating microRNA-185 and downregulating KLK5.Cell death & disease · 2020Article
- MicroRNAs and Corresponding Targets in Esophageal Cancer as ShownCancer genomics & proteomicsReview
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance, whether intrinsic or acquired, often leads to treatment failure in esophageal squamous cell carcinoma (ESCC). Clarifying the mechanism of drug resistance in ESCC has great significance for reversing drug resistance, as well as improving the prognosis of patients. Previously, we demonstrated that etoposide-induced 2.4-kb mRNA (EI24) is the target of miR-483-3p, which promoted the growth, migration, and drug resistance in ESCC, suggesting that EI24 participates in repressing the tumorigenesis and progression of ESCC. Here, we observed that EI24 was remarkably decreased in ESCC tissues. Moreover, its expression was directly linked to the prognosis of patients. We then confirmed that the forced overexpression of EI24 repressed cell growth and sensitized ESCC cells to chemotherapeutic agents, whereas EI24 silencing had the opposite effect. Furthermore, gene microarray and ingenuity pathway analysis (IPA) were performed to establish the potential mechanisms and indicated that EI24 exerts a tumor-suppressive role via suppressing the acute phase response signaling pathway or IL-1 signaling pathway in ESCC. Collectively, our data reveal that EI24 overexpression attenuates malignant phenotypes of ESCC and that it is a novel possible ESCC therapeutic target.
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