Epigenetic Regulation in Colorectal Cancer
Summary
Epigenetic regulation in colorectal cancer encompasses heritable alterations in gene expression without changes to the underlying DNA sequence. Principal mechanisms include DNA methylation at CpG dinucleotides, post-translational histone modifications and the influence of non-coding RNAs on chromatin structure. In colorectal carcinogenesis, aberrant hypermethylation of promoter CpG islands silences tumour suppressor genes such as SFRP family members and others involved in cell adhesion, apoptosis and DNA repair. Conversely, global hypomethylation can activate oncogenes and destabilise genomic integrity. Histone marks, notably alterations in acetylation at H3K27 and methylation at H3K4 and H3K9, reshape enhancer and promoter landscapes to favour malignant transcriptional programmes. These changes often intersect with key pathways, such as Wnt/β-catenin signalling, microsatellite instability and the CpG island methylator phenotype (CIMP), contributing to tumour initiation, progression and therapeutic resistance. Epigenetic alterations are reversible and offer avenues for biomarker development in early detection, prognostic stratification and response prediction. Advances in high-throughput profiling and single-cell technologies are refining our understanding of tumour heterogeneity and epigenetic evolution, thereby informing the rational design of epigenetic therapies and precision oncology strategies.
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Epigenetic Regulation in Colorectal Cancer publication trend
The graph below shows the total number of articles in epigenetic regulation in colorectal cancer across all publications each year (not limited to Nature Index journals).
Technical terms
DNA methylation: covalent addition of methyl groups to cytosine bases in CpG dinucleotides, commonly leading to transcriptional repression.
CpG island methylator phenotype (CIMP): a subtype of tumours characterised by widespread hypermethylation of promoter CpG islands and silencing of multiple tumour suppressor genes.
Promoter hypermethylation: dense methylation of gene promoter regions, which blocks transcription factor binding and downregulates gene expression.
Histone modification: chemical alterations (e.g., acetylation, methylation) to histone tails that regulate chromatin compaction and accessibility of DNA to transcriptional machinery.
Epigenetic clock: predictive algorithms that estimate biological age of tissues by measuring methylation levels at specific CpG sites.
References
- Developing survival prediction models in colorectal cancer using epigenome-wide DNA methylation data from whole blood. npj Precision Oncology (2024).
- Forkhead box E1, frequently downregulted by promoter methylation, inhibits colorectal cancer cell growth and migration. Cancer Cell International (2024).
- Dysfunctional epigenetic aging of the normal colon and colorectal cancer risk. Clinical Epigenetics (2020).
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