Epigenetic Regulation of MicroRNA Expression in Human Cancers
Summary
Epigenetic mechanisms, including DNA methylation and histone modifications, play a pivotal role in governing microRNA (miRNA) expression programmes during oncogenesis. Aberrant hypermethylation of miRNA gene promoters frequently silences tumour-suppressive miRNAs, facilitating unchecked proliferation, evasion of apoptosis and metastatic progression. Conversely, global hypomethylation can activate oncogenic miRNAs, disrupting normal gene networks. Histone-modifying enzymes, such as Polycomb group proteins, establish repressive chromatin marks at miRNA loci, further shaping the non-coding transcriptome in diverse malignancies. Reciprocal feedback loops between miRNAs and epigenetic regulators—whereby miRNAs target DNA methyltransferases or histone modifiers—add an additional layer of control. Together, these interconnected pathways modulate cellular identity, influence drug response and present both biomarkers of disease state and targets for novel therapeutic intervention.
Research from Nature Portfolio
Recent studies have shown that DNA methylation at regions flanking primary miRNA transcripts enhances their processing into mature species. Methyl-CpG binding protein 2 (MeCP2) binds to methylated miRNA loci, pauses RNA polymerase II elongation and promotes Drosha-mediated cleavage. This direct link between DNA methylation and miRNA biogenesis reveals how epigenetic modifications can selectively amplify miRNAs with oncogenic potential and suggests new avenues for modulating miRNA levels in cancer therapy.
Epigenetic Regulation of MicroRNA Expression in Human Cancers publication trend
The graph below shows the total number of articles in epigenetic regulation of microrna expression in human cancers across all publications each year (not limited to Nature Index journals).
Technical terms
Epigenetic regulation: Heritable alterations in gene expression not involving changes to the DNA sequence.
DNA methylation: Covalent addition of methyl groups to cytosine residues in CpG dinucleotides, leading to chromatin compaction and transcriptional silencing.
DNMTs: DNA methyltransferase enzymes responsible for establishing and maintaining DNA methylation patterns.
Histone modification: Post-translational chemical alterations of histone proteins that influence chromatin structure and gene activity.
MicroRNA (miRNA): Small non-coding RNA molecules that regulate target mRNA stability and translation.
EZH2: A histone methyltransferase component of Polycomb repressive complex 2 that mediates tri-methylation of histone H3 lysine 27.
MeCP2: A methyl-CpG-binding protein that recognises methylated DNA and recruits factors to modulate transcription and RNA processing.
Drosha: A nuclear RNase III enzyme that cleaves primary miRNA transcripts into precursor miRNAs for further maturation.
References
- The Mechanism of DNA Methylation and miRNA in Breast Cancer. International Journal of Molecular Sciences (2023).
- Estrogen-mediated DNMT1 and DNMT3A recruitment by EZH2 silences miR-570-3p that contributes to papillary thyroid malignancy through DPP4. Clinical Epigenetics (2024).
- DNA methylation directs microRNA biogenesis in mammalian cells. Nature Communications (2019).
- Regulatory Mechanisms of Epigenetic miRNA Relationships in Human Cancer and Potential as Therapeutic Targets. Cancers (2020).
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