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Transcriptomics-Based Repositioning of Natural Compound, Eudesmin, as a PRC2 Modulator.

Sang Ah Yi¹, Ki Hong Nam¹, Min Gyu Lee¹

¹School of Pharmacy, Sungkyunkwan University, Suwon 16419, Korea.

Molecules (Basel, Switzerland)

|September 28, 2021

Summary

Eudesmin treatment enriches Polycomb Repressive Complex 2 (PRC2) target genes, downregulating Wnt signaling and maintaining stem cell pluripotency. This study reveals eudesmin

Keywords:

eudesmin pluripotency polycomb repressive complex 2 transcriptome wnt

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Area of Science:

Epigenetics
Stem Cell Biology
Molecular Pharmacology

Background:

Extensive epigenetic remodeling is crucial for stem cell fate determination.
Eudesmin was previously found to regulate mesenchymal stem cell lineage commitment by inhibiting signaling molecules.
Genomewide epigenetic changes induced by eudesmin were not previously characterized.

Purpose of the Study:

To investigate the genomewide epigenetic modulations induced by eudesmin treatment in stem cells.
To identify the role of Polycomb Repressive Complex 2 (PRC2) in eudesmin-mediated epigenetic regulation.
To elucidate the impact of eudesmin on Wnt signaling and stem cell pluripotency.

Main Methods:

Transcriptome profiling to identify PRC2 target genes affected by eudesmin.
Gene Ontology (GO) analysis to determine the functional pathways of downregulated PRC2 target genes.
Chromatin Immunoprecipitation followed by quantitative PCR (ChIP-qPCR) and reverse transcription quantitative PCR (RT-qPCR) to analyze PRC2 occupancy and gene expression.
Analysis of Gene Expression Omnibus (GEO) profiles to compare gene expression patterns.

Main Results:

Eudesmin treatment led to the enrichment of PRC2 target genes.
Downregulated PRC2 target genes were associated with Wnt signaling and pluripotency pathways, with DKK1 identified as a key hub gene.
Eudesmin treatment increased PRC2 component (EZH2, SUZ12) occupancy and H3K27me3 levels at the DKK1 promoter, suppressing its transcription.
Gene expression changes induced by eudesmin showed an inverse pattern to those caused by Oct4 depletion, with upregulation of pluripotency markers (Oct4, Sox2, Nanog).

Conclusions:

Pharmacological modulation of PRC2 dynamics by eudesmin can control Wnt signaling.
Eudesmin treatment promotes the maintenance of stem cell pluripotency.
These findings highlight a novel mechanism by which eudesmin influences stem cell fate through epigenetic regulation of PRC2.