ArticleJournal of Cancer2022
EGLN1 induces tumorigenesis and radioresistance in nasopharyngeal carcinoma by promoting ubiquitination of p53 in a hydroxylase-dependent manner.
Article in Journal of Cancer, 2022. 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, 11 citations in OpenAlex.
- Exploring the prognostic value and immune landscape of EGLN1 in colorectal cancer: insights from bioinformatics analysis.Discover oncology · 2025Article
- Article
- Prolyl 4-hydroxylase subunit alpha-2 acts as a TRIM21 ubiquitination substrate to promote papillary thyroid cancer progression via the glycolytic pathway.Cell death & disease · 2025Article
- Validation and the role of PDK4 relevant to ferroptosis in degenerative lumbar disc disease.Journal of orthopaedic surgery and research · 2025Article
- Causal associations between circulating protein ratios and drug resistance in papillary thyroid cancer: a Mendelian randomization study.Discover oncology · 2025Article
- An early-stage 3D fibroblast-featured tumor model mimics the gene expression of the naïve tumor microenvironment, including genes involved in cancer progression and drug resistance.Frontiers in oncology · 2025Article
- Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway.Biomedical reports · 2024Article
- Knockdown of cullin 3 inhibits progressive phenotypes and increases chemosensitivity in cholangiocarcinoma cells.Molecular medicine reports · 2024Article
- Understanding Hypoxia-Driven Tumorigenesis: The Interplay of HIF1A, DNA Methylation, and Prolyl Hydroxylases in Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2024Article
- Advances in prognostic models for osteosarcoma risk.Heliyon · 2024Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Egl-9 Family Hypoxia Inducible Factor 1 (EGLN1) is a proline hydroxylase mediating degradation of hypoxia-inducible factor α (HIFα) through the ubiquitination system. Studies have indicated an essential role for EGLN1 in angiogenesis and tumorigenesis. However, there is no consensus on the regulation of EGLN1 and its mechanism of action on nasopharyngeal carcinoma (NPC). This study explored the association of the expression of EGLN1 with characteristics of NPC tumors and its underlying mechanism. We found that the expression of EGLN1 showed a positive correlation with tumor T classification and clinical staging of patients with NPC. EGLN1 could promote cell proliferation, invasion and migration, and even enhance the cancer stem cells (CSCs) prosperity and radioresistance of NPC cells. Mechanistically, EGLN1 facilitated degradation of tumor protein p53 through the ubiquitination system. This effect could be weakened in the presence of dimethyloxalylglycine (DMOG), suggesting that EGLN1 down-regulated p53 based on its hydroxylase activity. In conclusion, overexpression of EGLN1 promoted oncogenesis and induced a CSC-like phenotype in NPC cells, then enhancing the ability for radioresistance by interacting with p53 in a hydroxylase-dependent manner. Thus, EGLN1 might serve as a potential therapeutic target for NPC.
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