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Updated: Jul 20, 2026

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
Published on: August 5, 2022
Targeting DNA methylation in cancer
1Department of Pharmacology and Therapeutics, McGill University, 3655 Sir William Osler Promenade, Montreal PQ H3G 1Y6 Canada. moshe.szyf@mcgill.ca
Abstract:
Cancer growth and metastasis require the coordinate change in gene expression of different sets of genes. While genetic alterations can account for some of these changes, many of the changes in gene expression observed in cancer are caused by epigenetic modifications. The epigenome consists of the chromatin and its modifications, the "histone code" as well as the pattern of distribution of covalent modifications of cytosines residing in the dinucleotide sequence CG by methylation. The normal pattern of distribution of DNA methylation is altered in cancer. A number of genes are regionally hypermethylated but many parts of the genome are hypomethylated. Hypermethylation of tumor suppressor genes is involved in silencing of strategic genes. DNA hypermethylation has received much attention and a number of clinical trials are underway with different inhibitors of DNA methylating enzymes. It is now becoming clear however that hypomethylation also plays a role in cancer by activating genes required for invasion and metastasis. The potential therapeutic implications of targeting DNA methylation in cancer are discussed.
Insights
Epigenetic modifications, including DNA methylation changes, drive cancer progression. Both DNA hypermethylation and hypomethylation play critical roles in cancer development and metastasis, offering therapeutic targets.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Background:
- Cancer development involves altered gene expression.
- Epigenetic modifications, such as DNA methylation, significantly influence gene expression in cancer.
- The epigenome, including histone modifications and DNA methylation patterns, is crucial for cellular function.
Purpose of the Study:
- To explore the role of epigenetic modifications, specifically DNA methylation, in cancer growth and metastasis.
- To differentiate the roles of DNA hypermethylation and hypomethylation in tumorigenesis.
- To discuss the therapeutic potential of targeting DNA methylation in cancer treatment.
Main Methods:
- Review of existing literature on cancer epigenetics and DNA methylation.
- Analysis of gene expression changes associated with epigenetic modifications in cancer.
- Examination of the impact of DNA methylation patterns on tumor suppressor genes and invasion-related genes.
Main Results:
- Cancer progression is linked to altered DNA methylation patterns, including regional hypermethylation and genome-wide hypomethylation.
- Hypermethylation of tumor suppressor genes leads to their silencing.
- Hypomethylation contributes to the activation of genes promoting invasion and metastasis.
Conclusions:
- Epigenetic alterations, particularly in DNA methylation, are fundamental to cancer.
- Both hypermethylation and hypomethylation are critical mechanisms in cancer, with distinct roles in gene silencing and activation of pro-metastatic genes.
- Targeting DNA methylation pathways presents a promising therapeutic strategy for cancer treatment.
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