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SAM-DNMT3A, a strategy for induction of genome-wide DNA methylation, identifies DNA methylation as a vulnerability in ER-positive breast cancers
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SAM-DNMT3A, a strategy for induction of genome-wide DNA methylation, identifies DNA methylation as a vulnerability in ER-positive breast cancers
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Journal Article
SAM-DNMT3A, a strategy for induction of genome-wide DNA methylation, identifies DNA methylation as a vulnerability in ER-positive breast cancers
2024
Overview
DNA methylation is an epigenetic mark that plays a critical role in regulating gene expression. DNA methyltransferase (DNMT) inhibitors, inhibit global DNA methylation and have been a key tool in studies of DNA methylation. A major bottleneck is the lack of tools to induce global DNA methylation. Here, we engineered a CRISPR based approach, that we initially designed, to enable site-specific DNA methylation. Using the synergistic activation mediator (SAM) system, we unexpectedly find that regardless of the targeted sequence any sgRNA induces global genome-wide DNA methylation. We term this method SAM-DNMT3A and show that induction of global DNA methylation is a unique vulnerability in ER-positive breast cancer suggesting a therapeutic approach. Our findings highlight the need of caution when using CRISPR based approaches for inducing DNA methylation and demonstrate a method for global induction of DNA methylation.
DNA methylation is an epigenetic mark that plays a critical role in many biological processes. Here, we describe the development of SAM-DNMT3A a tool for induction of genome wide DNA methylation. Using SAM-DNMT3A we show that DNA methylation is a unique vulnerability in ER+ breast cancer.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
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/ Breast Neoplasms - drug therapy
/ Breast Neoplasms - metabolism
/ CRISPR
/ DNA
/ DNA (Cytosine-5-)-Methyltransferases - genetics
/ DNA (Cytosine-5-)-Methyltransferases - metabolism
/ DNA Methyltransferase 3A - metabolism
/ Female
/ Gene Expression Regulation, Neoplastic
/ Genomes
/ Humanities and Social Sciences
/ Humans
/ Receptors, Estrogen - genetics
/ Receptors, Estrogen - metabolism
/ RNA, Guide, CRISPR-Cas Systems - genetics
/ Science
