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Updated: Dec 31, 2025
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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Mdig promotes oncogenic gene expression through antagonizing repressive histone methylation markers
Qian Zhang1, Chitra Thakur1, Yao Fu1
1Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, 259 Mack Avenue, Detroit, MI 48201, USA.
Theranostics
|January 7, 2020
Summary
The mineral dust-induced gene (mdig) antagonizes repressive histone methylation, impacting cancer pathways. Depleting mdig increases histone trimethylation, suggesting mdig as a potential cancer therapy target.
Area of Science:
- Molecular Biology
- Epigenetics
- Cancer Research
Background:
- The mineral dust-induced gene (mdig) is overexpressed in human cancers.
- Its role in histone demethylation remains unclear, despite other JmjC-domain proteins having this activity.
Purpose of the Study:
- To investigate the role of mdig in histone methylation.
- To provide evidence for mdig's involvement in demethylation processes.
Main Methods:
- CRISPR-Cas9 gene editing to create mdig knockout cell lines.
- Analysis of histone methylation profiles using global methylation analysis.
- Chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing (RNA-seq).
Main Results:
- Mdig depletion led to increased repressive histone trimethylation (H3K9me3, H3K27me3, H4K20me3) in multiple cell types.
- Genetic disruption of mdig enriched repressive histone trimethylation.
- Inhibition of target genes involved in cell growth, stemness, fibrosis, and motility was observed.
Conclusions:
- This study offers the first insight into mdig's function as an antagonist of repressive histone methylation markers.
- Targeting mdig presents a novel therapeutic strategy for cancer treatment.
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