ArticleMolecular cancer therapeutics2025
Blockade of the PGE2 Pathway Inhibits the Growth of PTEN-Deficient HNSCC Tumors.
Article in Molecular cancer therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- HGF/c-MET signaling induces glutamine metabolism in MET-amplified head and neck squamous cell carcinoma via MAPK/ERK-dependent induction of GLS-1.Medical oncology (Northwood, London, England) · 2026Article
- Conventional and alternative approaches for targeting PIK3CA and PTEN alterations in head and neck, breast, and other cancers.Advances in biological regulation · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Increased PI3K signaling as a result of PIK3CA mutation or amplification or decreased expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is one of the most common alterations in head and neck squamous cell carcinoma (HNSCC). PTEN negatively regulates PI3K signaling and its downstream effectors including COX2. COX2 mediates the synthesis of prostaglandin E2 (PGE2) which contributes to immunosuppression in the tumor microenvironment. PGE2 also binds to one or more EP receptors (EP1-EP4) and promotes the growth of tumor cells via activation of EP2 and EP4. However, the role of PGE2 in PTEN-deficient HNSCC is incompletely understood. In this study, we assessed PGE2 signaling in PTEN-deficient HNSCC and evaluated the effect of aspirin or TPST-1495, a dual EP2/EP4 antagonist, on the growth of PTEN knockout and PIK3CA-altered HNSCC tumors in immunocompetent mice. Our results demonstrated that aspirin selectively inhibits the growth of PTEN knockout HNSCC tumors. TPST-1495 inhibited tumor growth and substantially increased the antitumor activity of the immune checkpoint inhibitor anti-PD1. To date, there are no FDA-approved therapies for PI3K pathway-altered HNSCC. Our findings suggest that NSAIDs demonstrate antitumor activity in PTEN-deficient or PI3K-altered tumors whereas EP2/EP4 targeting may augment FDA-approved anti-PD1 therapy in HNSCC.
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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 Socratic graph.