Related Experiment Video

Updated: Jan 18, 2026

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
06:07

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors

Published on: August 5, 2022

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Transcription factors overcome the repressive impact of Polycomb-associated methylation in tumors

Min-Kyeong Kwon, Goeun Park, Dayoung Go

    Biorxiv : the Preprint Server for Biology
    |June 6, 2025
    PubMed

    Insights

    DNA methylation changes in colorectal cancer (CRC) don't always silence genes. Polycomb-marked genes can remain active despite DNA hypermethylation, suggesting epigenetic plasticity drives cancer progression.

    Area of Science:

    • Epigenetics and Genomics
    • Cancer Biology
    • Molecular Oncology

    Background:

    • DNA methylation is a crucial epigenetic mechanism frequently altered in cancer.
    • Understanding how DNA methylation dynamics influence gene expression during cancer progression is essential.
    • Colorectal cancer (CRC) exhibits significant epigenetic dysregulation.

    Purpose of the Study:

    • To investigate the relationship between DNA methylation patterns and gene expression in colorectal cancer.
    • To map promoter methylation and gene expression dynamics in paired tumor and non-tumor tissues.
    • To elucidate the role of Polycomb group (PcG) occupancy in mediating methylation-driven transcriptional changes.

    Main Methods:

    • Targeted bisulfite sequencing to analyze DNA methylation.
    • RNA sequencing (RNA-seq) to assess gene expression levels.
    • Analysis of paired tumor and non-tumor tissues from 80 Korean colorectal cancer patients.

    Main Results:

    • Promoter methylation patterns showed dynamic shifts between non-tumor and tumor tissues.
    • Changes in DNA methylation did not consistently correlate with gene silencing or activation.
    • Polycomb-marked (PcG+) promoters were prone to hypermethylation but often retained transcriptional activity in tumors, particularly for transcription factor (TF) genes.
    • Hypermethylation in non-PcG-marked (PcG-) promoters was more consistently linked to transcriptional repression.

    Conclusions:

    • Epigenetic plasticity at PcG+ TF gene promoters can overcome the repressive effects of DNA methylation in colorectal cancer.
    • Tumors may leverage this plasticity to maintain or enhance the expression of key regulatory genes.
    • PcG occupancy is critical in determining the functional impact of DNA methylation changes during colorectal tumorigenesis.

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