ArticleImmunology letters2016
Indomethacin sensitizes resistant transformed cells to macrophage cytotoxicity.
Article in Immunology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Targeting the Vim-PGIHuman mutation · 2026Article
- Immunoregulatory mechanisms of the arachidonic acid pathway in cancer.FEBS letters · 2025Review
- Machine Learning-Driven Prediction, Preparation, and Evaluation of Functional Nanomedicines Via Drug-Drug Self-Assembly.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Macrophage metabolism, phenotype, function, and therapy in hepatocellular carcinoma (HCC).Journal of translational medicine · 2023Review
- Carrier-free nanoplatforms from natural plants for enhanced bioactivity.Journal of advanced research · 2023Review
- Self-assembled nanoformulations of paclitaxel for enhanced cancer theranostics.Acta pharmaceutica Sinica. B · 2023Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Activated macrophages are well known to exhibit anti-tumor properties. However, certain cell types show intrinsic resistance. Searching for a mechanism that could explain this phenomenon, we observed that the supernatant of resistant cells could confer resistance to otherwise sensitive tumor cells, suggesting the presence of a secreted suppressor factor. The effect was abolished upon dialysis, indicating that the suppressor factor has a low molecular weight. Further studies showed that prostaglandin E2 (PGE2) is secreted by the resistant tumor cells and that inhibition of PGE2 production by indomethacin, a cyclooxygenase (COX) inhibitor, eliminated the macrophage suppression factor from the supernatant, and sensitized the resistant tumor cells to macrophage cytotoxicity. This study emphasizes the important role of tumor-secreted PGE2 in escaping macrophage surveillance and justifies the use of COX inhibitors as an adjuvant for improving tumor immunotherapy.
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Registered trials
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