ArticleInternational journal of general medicine2023
IDO1 Promotes the Progression of NSCLC by Regulating the Polarization of M2 Macrophages.
Article in International journal of general medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Vitexin antagonizes the kynurenine pathway via AhR inhibition to reprogram tumor-associated macrophages and enhance antitumor immunity in lung adenocarcinoma.Molecular and cellular biochemistry · 2026Article
- Precision engineering of macrophage reprogramming with RNA interference-loaded lipid nanoparticles: a game-changer in cancer immunotherapy.Drug delivery and translational research · 2026Review
- Macrophages in lung cancer: principal factors, regulatory mechanisms, and therapeutic opportunities: a narrative review.Translational lung cancer research · 2026Review
- ID1 in TAMs promoted the progression of non-small-cell carcinoma via increasing NF-κB/NPM1/SHP1/SHP2 signaling induced M2 polarization.Scientific reports · 2026Article
- Bicaudal‑C1 in Cancer: Molecular Mechanisms and Therapeutic Strategies Integrating Chinese and Western Medicine.Drug design, development and therapy · 2026Review
- M2 macrophage-derived exosomes promote cell proliferation, migration and EMT of non-small cell lung cancer by secreting miR-155-5p.Molecular and cellular biochemistry · 2025Article
- Expression of immune checkpoints (IDO and PD-L1) in oral tongue cancer patients: a 10-year retrospective cohort study in Pakistan.Frontiers in oncology · 2025Article
- Tumor-Associated Macrophages as Major Immunosuppressive Cells in the Tumor Microenvironment.Cancers · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Non-small cell lung cancer (NSCLC) is currently a problem in the clinic and in society. Tumor-related macrophages (TAMs) in the tumor microenvironment (TME) play a vital role in the development of NSCLC. Patients and Methods: Bioinformatics was used to analyze the role of Indoleamine 2,3-dioxygenase 1 (IDO1) in NSCLC and the correlation of its expression with CD163 expression. The expression of CD163 and IDO1 was measured by immunohistochemistry, and their colocalization was assessed by immunofluorescence. M2 macrophage polarization was induced, and a coculture model of NSCLC cells and macrophages was established. Results: Bioinformatics analysis showed that IDO1 promoted the metastasis and differentiation of NSCLC and inhibited DNA repair. Moreover, the expression of IDO1 was positively correlated with CD163 expression. We discovered that IDO1 expression was related to M2 macrophage differentiation. In vitro, we showed that increased IDO1 expression promoted the invasion, proliferation, and metastasis of NSCLC cells. Conclusion: In conclusion, we determined that IDO1 can regulate the M2 polarization of TAMs and promote the progression of NSCLC, which provides partial theoretical evidence for the use of IDO1 inhibitors in the treatment of NSCLC.
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