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Navigating the DNA methylation landscape of cancer

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TRENDS IN GENETICS
卷 37, 期 11, 页码 1012-1027

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CELL PRESS
DOI: 10.1016/j.tig.2021.05.002

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DNA methylation is a chemical modification that defines cell type and lineage through controlling gene expression and genome stability. Aberrant DNA methylation in cancer cells targets CpG islands in gene expression regulatory elements. Recent studies suggest that the classical model of DNA hypermethylation in cancer needs to be reevaluated.
DNA methylation is a chemical modification that defines cell type and lineage through the control of gene expression and genome stability. Disruption of DNA methylation control mechanisms causes a variety of diseases, including cancer. Cancer cells are characterized by aberrant DNA methylation (i.e., genome-wide hypomethylation and site-specific hypermethylation), mainly targeting CpG islands in gene expression regulatory elements. In particular, the early findings that a variety of tumor suppressor genes (TSGs) are targets of DNA hypermethylation in cancer led to the proposal of a model in which aberrant DNA methylation promotes cellular oncogenesis through TSGs silencing. However, recent genome-wide analyses have revealed that this classical model needs to be reconsidered. In this review, we will discuss the molecular mechanisms of DNA methylation abnormalities in cancer as well as their therapeutic potential.

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