ArticleCell death discovery2023
IDO1 facilitates esophageal carcinoma progression by driving the direct binding of NF-κB and CXCL10.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Ido1 or Ido2 deficiency in myeloid-derived cells attenuates TMEV-induced ictogenesis.Journal of neuroimmunology · 2025Article
- Microglia-specific Ido2 deficiency attenuates ictogenesis in the TMEV model of viral encephalitis.Brain, behavior, and immunity · 2025Article
- Exploring metabolic reprogramming in esophageal cancer: the role of key enzymes in glucose, amino acid, and nucleotide pathways and targeted therapies.Cancer gene therapy · 2025Review
- Post-translational governance of NF-κB in cancer immunity: mechanisms and therapeutic horizons.Frontiers in immunology · 2025Review
- Low Indoleamine 2,3-Dioxygenase 1 Expression Enhances Dendritic Cells Response to Tumor Cells Against Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2025Article
- IDO and TDO inhibitors in cancer immunotherapy: mechanisms, clinical development, and future directions.Frontiers in pharmacology · 2025Review
- Integrated analyses reveal IDO1 as a prognostic biomarker coexpressed with PD-1 on tumor-associated macrophages in esophageal squamous cell carcinoma.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal carcinoma (EC), one of the most lethal human malignancies, lacks effective targeted therapies. Indoleamine 2,3-dioxygenase 1 (IDO1) plays a key role in a variety of cancers, but its role and mechanism in EC are still unclear. Immunohistochemistry and qRT-PCR were used to analyze the expression of IDO1 in EC, and the prognostic value of IDO1 in EC was evaluated by Kaplan-Meier test. The in vitro and in vivo function loss/acquisition tests were performed to evaluate the biological effects of IDO1 in EC. The mechanism of action of IDO1-regulation EC was explored through Firefly luciferase & Renilla luciferase activity reporter, chromatin immunoprecipitation (ChIP) and immunofluorescence (IF) assays. Clinically, IDO1 expression was abnormally elevated in EC and positively correlated with overall survival. Functionally, IDO1 was contributed to the proliferation and migration of EC cells. Mechanically, IDO1 regulated the expression of chemokine C-X-C ligand 10 (CXCL10) by promoting the entry of NF-κB into the nucleus to combine with the promoter of CXCL10. Consistently, IDO1 facilitated EC progression may dependent on the presence of CXCL10. Moreover, NF-κB alleviated the inhibitory effect of IDO1 knockdown on EC. IDO1 drove the progression of EC by directly binding NF-κB and CXCL10, the finding that may provide an effective theoretical basis for precise therapies for EC.
Identifiers
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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.