ArticleActa pharmacologica Sinica2026
Epigenetic regulation of NDGA and its synergistic inhibition with EZH2 inhibitors in prostate cancer via NRP1.
Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic modulating drugs are emerging as promising cancer treatments. We previously showed that a natural compound, nordihydroguaiaretic acid (NDGA), exerted anti-prostate cancer effects in vitro and in vivo. In this study, we elucidated the anticancer mechanisms of NDGA against prostate cancer. Using integrating bioinformatics analysis and proteomic research, we identified 12 differentially expressed proteins in NDGA-treated PC3 cells that were associated with EZH2, a histone methyltransferase and a catalytic component of polycomb repressive complex 2 (PRC2), which catalyzed the trimethylation of histone H3 at Lys27 (H3K27me3). We showed that NDGA (5, 10, 20 μmol/L) dose-dependently inhibited EZH2 expression in PC3 cells by increasing its degradation and inhibiting its transcription. We demonstrated that NDGA targeted neuropilin 1 (NRP1) in PC3 cells, inhibiting the EZH2/H3K27me3 and PI3K/AKT/mTOR pathways and the expression of E2F1. NDGA blocked E2F1 binding to the EZH2 promoter, decreasing EZH2 and H3K27me3 levels. On the other hand, NDGA inhibited CBP/p300, decreased H3K27ac levels, and synergized with the EZH2 inhibitor EPZ6438 against PC3 cells. In conclusion, NDGA is a potential epigenetic antineoplastic agent that downregulates EZH2 and H3K27me3 through the NRP1 and PI3K/AKT/mTOR pathways and exerts a synergistic antitumor effect with H3K27ac and EZH2 inhibitors, suggesting that it could be a valuable therapeutic option for prostate cancer.
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.