ArticleInternational journal of oncology2018
EPB41L3 is a potential tumor suppressor gene and prognostic indicator in esophageal squamous cell carcinoma.
Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed, 47 citations in OpenAlex.
- EPB41L family serves as a prognostic biomarker for kidney renal clear cell carcinoma.Cell adhesion & migration · 2026Article
- Increased vulnerability of colorectal cancer models with high alkylation damage to NTHL1 inactivation.Scientific reports · 2026Article
- Multi-layered molecular profiling informs the diagnosis and targeted therapy of desmoplastic small round cell tumor.Nature communications · 2026Article
- EPB41L3 Inhibits the Progression of Cervical Cancer Via the ERK/p38 MAPK Signaling Pathway.Molecular biotechnology · 2025Article
- Insight into the role of DNA methylation in prognosis and treatment response prediction of gastrointestinal cancers.Epigenomics · 2025Review
- Data-Driven Identification of Early Cancer-Associated Genes via Penalized Trans-Dimensional Hidden Markov Models.Biomolecules · 2025Article
- Clinical Proteomics Reveals Vulnerabilities in Noninvasive Breast Ductal Carcinoma and Drives Personalized Treatment Strategies.Cancer research communications · 2025Article
- Extensive immunophenotypic sub-population analysis of StemRegenin1 expanded haematopoietic stem/progenitor cells.Stem cell research & therapy · 2024Article
- Regulation ofWorld journal of clinical oncology · 2024Article
- Dual role of CASP8AP2/FLASH in regulating epithelial-to-mesenchymal transition plasticity (EMP).Translational oncology · 2024Article
- Exploring the multifaceted role of direct interaction between cancer cells and fibroblasts in cancer progression.Frontiers in molecular biosciences · 2024Review
- Downregulation of complement factor H attenuates the stemness of MDA‑MB‑231 breast cancer cells via modulation of the ERK and p38 signaling pathways.Oncology letters · 2023Article
- Assessing the risk of cervical neoplasia in the post-HPV vaccination era.International journal of cancer · 2023Review
- Digital spatial profiling of human parathyroid tumors reveals cellular and molecular alterations linked to vitamin D deficiency.PNAS nexus · 2023Article
- Classification related to immunogenic cell death predicts prognosis, immune microenvironment characteristics, and response to immunotherapy in lower-grade gliomas.Frontiers in immunology · 2023Article
- Induced resistance to ifosfamide in osteosarcoma cells suggests a more aggressive tumor profile.Biochemistry and biophysics reports · 2022Article
- Kozak Similarity Score Algorithm Identifies Alternative Translation Initiation Codons Implicated in Cancers.International journal of molecular sciences · 2022Article
- HDAC10 Inhibits Cervical Cancer Progression through Downregulating the HDAC10-microRNA-223-EPB41L3 Axis.Journal of oncology · 2022Article
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Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Although there have been reports about the role of erythrocyte membrane protein band 4.1 like 3 (EPB41L3) in several types of cancer, primarily in non-small-cell lung carcinoma, the molecular function and modulatory mechanisms of EPB41L3 remain unclear. In specific, the functional and clinical significance of EPB41L3 in esophageal squamous cell carcinoma (ESCC) has not been explored to date. In the present study, reduced EPB41L3 expression was demonstrated in ESCC cell lines and tissues, which was due to its high methylation rate. Ectopic expression of EPB41L3 in ESCC cells inhibited cell proliferation in vivo and in vitro. In addition, EPB41L3 overexpression induced apoptosis and G2/M cell cycle arrest by activating Caspase-3/8/9 and Cyclin-dependent kinase 1/Cyclin B1 signaling, respectively. Notably, patients with higher EPB41L3 expression had markedly higher overall survival rates compared with patients with lower EPB41L3 expression. In summary, the present results suggest that EPB41L3 may be a tumor suppressor gene in ESCC development, representing a potential therapeutic target and a prognostic indicator for ESCC.
Identifiers
What OpenQuestion holds
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.