ArticleFrontiers in pharmacology2025
Article in Frontiers in pharmacology, 2025. 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
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
6 citing papers in PubMed.
- The bidirectional immunoregulatory effects of Traditional Chinese Medicine on the cGAS-STING signaling pathway and their translational prospects.Chinese medicine · 2026Review
- Quercetin induces molecular hallmarks of immunogenic cell death and cGAS-STING pathway activation via mitochondrial DNA release in hepatocellular carcinoma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Unveiling the sensing potential of innate lymphoid cells.Communications biology · 2026Review
- An Overview of the Phytochemistry, Biological Activities and Therapeutic Potential ofPlants (Basel, Switzerland) · 2026Review
- Self-Assembly of Stimuli-Responsive Peptide Enhances Therapeutics by Specifically Disrupting Hepatocellular Carcinoma Lysosomes In Vivo.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Baohuoside I CombatedAntioxidants (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Methods: The impact of EPE on NK cell activity was assessed via Enzyme-Linked Immunosorbent Assay (ELISA) and flow cytometry. A co-culture model of NK-92 cells with K562 target cells was constructed to evaluate EPE-enhanced NK cytotoxicity using Calcein-AM release assay. A murine HCC subcutaneous xenograft model was employed to demonstrate EPE-targeted NK cell activation against HCC Results: EPE significantly promoted the synthesis and release of IFN-γ, Granzyme B, and Perforin in NK-92 cells and increased the expression of the activating receptor NKG2D on the NK-92 cell and human primary NK cells surface. Treatment of human primary NK cells with EPE increased the proportion of the CD56 Conclusion: EPE exerts anti- HCC effects by activating NK cells through the activation of the cGAS-STING signaling pathway. This suggests that EPE may serve as a potential immunotherapeutic agent, offering novel therapeutic perspectives for the treatment of HCC.
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.