ArticleInternational journal of molecular sciences2026
Targeting Neuropeptide Y/DPP4 Signalling Suppresses Ewing Sarcoma Survival and Improves Monocyte Viability.
Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Neuropeptide Y in cancer metastasis and chemoresistance.Neuropeptides · 2026Review
- Integrated Immunotherapy Target Atlas for Ewing Sarcoma.Cancer genomics & proteomicsReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Survival rates for metastatic Ewing sarcoma (EwS) have remained persistently low over recent decades, highlighting the need for more effective chemotherapeutic options. Potential targets may be found within the Neuropeptide Y (NPY) signalling pathway that has been implicated in EwS cell survival. However, confounding factors include hypoxia that modulates NPY signalling, dipeptidyl peptidase-4 (DPP4/CD26) that cleaves NPY and interactions via NPY signalling from infiltrating immune cells. We investigated these interactions in A673 and SK-ES-1 EwS cell lines and THP-1 monocytes to identify therapeutic targets suitable for drug repurposing. Both EwS cell lines secreted NPY into conditioned media and extracellular vesicles. Recombinant NPY enhanced viability of both A673 and SK-ES-1 cells; however, the NPY1R antagonist BMS-193885 reduced viability in A673 cells only. Recombinant DPP4 widely promoted EwS viability and, under hypoxic conditions, it increased cell metabolism. The DPP4 inhibitor linagliptin, which is used clinically, consistently suppressed EwS viability with elevated sensitivity under hypoxia, where there was increased cell death of SK-ES-1 cells. Conversely, in THP-1 monocytes, NPY suppressed metabolism, BMS-193885 increased live-cell staining and DPP4 induced cell death. These findings suggest that NPY and DPP4 enhance EwS survival through autocrine/paracrine signalling while reducing monocyte viability. Thus, targeting the NPY/DPP4 signalling axis may provide therapeutic benefit by directly suppressing EwS growth and enhancing efficacy of immunotherapy.
Indexed as
Identifiers
What OpenQuestion holds
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.