ArticleCytoJournal2025
The mechanism of prostaglandin E2 upregulation of programmed death ligand 1 expression promoting immune escape in non-small cell lung cancer.
Article in CytoJournal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Non-small cell lung cancer (NSCLC) represents a major contributor to cancer-related mortality. This study aims to investigate the prostaglandin E synthase (PTGES) role in NSCLC, especially how prostaglandin E2 (PGE2), which is synthesized by PTGES prompts programmed death ligand 1 (PD-L1) expression, resulting in immune escape. Material and Methods: The PTGES and PGE2 expression levels were tested in normal and NSCLC samples, respectively. An A549 cell line that overexpressed and knocked down PTGES was established, and cell multiplication, colony formation, and aggression were evaluated. The PD-L1 levels and cytotoxicity effect of CD8 Results: The expression of PTGES in NSCLC cells notably increased compared with that in control cells ( Conclusion: This study confirmed that PGE2 promotes immune evasion of NSCLC by upregulating PD-L1, and the mechanism involves the activation of the PI3K/AKT/mTOR pathway. This research provides a novel theoretical basis for immunotherapy of NSCLC and emphasizes the clinical value of PTGES/PGE2 as a potential target.
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