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Unsafe SETs: histone lysine methyltransferases and cancer
Robert Schneider1, Andrew J Bannister, Tony Kouzarides
1Wellcome/Cancer Research UK Institute and Department of Pathology, Tennis Court Road, Cambridge, UK CB2 1QR.
Abstract:
Enzymes that covalently modify histones control many cellular processes by affecting gene expression. A new class of these enzymes is the histone lysine methyltransferase family, whose catalytic activity lies within a conserved domain, the SET domain. This article surveys the evidence for a connection between SET-domain-containing proteins and cancer. It proposes that deregulation of SET-domain function has an important role in carcinogenesis.
Insights
Histone modification enzymes regulate gene expression. This review explores how SET-domain proteins, a class of histone methyltransferases, are linked to cancer development and proposes their functional deregulation contributes to carcinogenesis.
Area of Science:
- Biochemistry
- Molecular Biology
- Epigenetics
Background:
- Enzymes covalently modifying histones are crucial regulators of cellular processes, particularly gene expression.
- The SET domain is a conserved catalytic domain found in histone lysine methyltransferases.
- Histone methylation patterns are critical for maintaining normal cellular function.
Purpose of the Study:
- To survey the existing evidence connecting SET-domain-containing proteins with cancer.
- To propose a role for the deregulation of SET-domain function in the process of carcinogenesis.
Main Methods:
- Literature review and evidence synthesis.
- Analysis of published studies on SET-domain proteins and their association with various cancers.
- Comparative analysis of normal and cancerous cellular contexts regarding SET-domain protein activity.
Main Results:
- Growing body of evidence suggests a significant association between SET-domain proteins and cancer.
- Specific SET-domain proteins are implicated as oncogenes or tumor suppressors.
- Dysregulation of SET-domain protein activity, including altered expression levels and catalytic function, is frequently observed in tumors.
Conclusions:
- SET-domain-containing proteins represent a critical link between epigenetic regulation and cancer.
- Deregulation of SET-domain function is proposed to be a key mechanism contributing to carcinogenesis.
- Targeting SET-domain proteins may offer novel therapeutic strategies for cancer treatment.