ArticleStem cell reports2025
A conserved function of EZH2-PRC2 in repression of primitive endoderm fate in mouse and human pluripotent cells.
Article in Stem cell reports, 2025. 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In early blastocyst, inner cell mass (ICM) undergoes a second wave of lineage commitment to generate epiblast (Epi) and primitive endoderm (PrE), restricting the developmental potential of their progeny. However, the epigenetic mechanism underlying this lineage segregation remains unclear. Here, we reveal that enhancer of zeste homolog 2 (EZH2) inhibition with EPZ-6438 transdifferentiates murine embryonic stem cells (ESCs) into primitive endoderm stem cells (PrESCs). Genetic ablation of Ezh2 in ESCs reduces the trimethylation of lysine 27 on histone 3 (H3K27me3) deposition at the promoters of PrE-specific genes, derepressing their expression and facilitating the PrESC conversion. Reconstitution with wild-type EZH2, but not catalytically inactive or EED-binding-deficient mutants in EZH2-deficient ESCs, blocks this transition. Strikingly, EZH2 inhibition reduces epiblast cell numbers in blastocysts, with 45.9% of embryos exhibiting ICMs composed of no SOX2-positive cells. Furthermore, EPZ-6438 treatment in human naive ESCs upregulates hypoblast-associated genes. In sum, these results reveal an evolutionarily conserved role for EZH2-polycomb repressive complex 2 (PRC2) in safeguarding pluripotency from primitive endoderm cell fate.
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.