DNA Methylation and Epigenetic Modifications in Esophageal Cancer
Summary
DNA methylation and epigenetic modifications play pivotal roles in the initiation and progression of esophageal cancer, encompassing both squamous cell carcinoma and adenocarcinoma. Methyl groups introduced into cytosine residues within CpG dinucleotides alter chromatin accessibility and gene expression without modifying the DNA sequence. Aberrant hypermethylation of promoter regions silences tumour suppressor genes and DNA repair pathways, while global hypomethylation promotes genomic instability and oncogene activation. Beyond DNA methylation, histone modifications such as acetylation and methylation of lysine residues contribute to chromatin remodelling and transcriptional regulation. Non-coding RNAs, including microRNAs and long non-coding RNAs, interact with epigenetic machinery to fine-tune gene expression networks. Collectively, these changes shape the tumour microenvironment, influencing cell proliferation, apoptosis, invasion and therapeutic resistance. Recent advances have elucidated key methylation signatures associated with early-stage disease and prognosis, and have spurred the development of non-invasive diagnostics based on circulating cell-free DNA. Furthermore, targeting epigenetic enzymes such as DNA methyltransferases and histone deacetylases has shown promise in sensitising tumours to chemoradiotherapy. An integrated understanding of epigenetic landscapes in esophageal cancer holds potential for improved biomarkers, stratified therapies and ultimately better patient outcomes.
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DNA Methylation and Epigenetic Modifications in Esophageal Cancer publication trend
The graph below shows the total number of articles in dna methylation and epigenetic modifications in esophageal cancer across all publications each year (not limited to Nature Index journals).
Technical terms
DNA methylation: Addition of a methyl group to cytosine in CpG dinucleotides, altering gene expression.
Promoter hypermethylation: Excessive methylation of gene promoter regions leading to transcriptional silencing.
Circulating cell-free DNA: Fragments of tumour-derived DNA detectable in plasma, used for non-invasive diagnostics.
Epigenetic silencing: Heritable repression of gene activity through DNA methylation or histone modification.
Histone modification: Covalent post-translational changes to histone proteins that influence chromatin structure and gene transcription.
Tumour microenvironment: Complex milieu of stromal cells, extracellular matrix and signalling molecules surrounding a tumour.
References
- Non-invasive diagnosis of esophageal cancer by a simplified circulating cell-free DNA methylation assay targeting OTOP2 and KCNA3: a double-blinded, multicenter, prospective study. Journal of Hematology & Oncology (2024).
- Decreased plasma gelsolin fosters a fibrotic tumor microenvironment and promotes chemoradiotherapy resistance in esophageal squamous cell carcinoma. Journal of Biomedical Science (2024).
- Epigenetic silencing of ZNF132 mediated by methylation-sensitive Sp1 binding promotes cancer progression in esophageal squamous cell carcinoma. Cell Death & Disease (2018).
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