Related Experiment Video

Updated: Jan 31, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
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Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

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SETting the Stage for Cancer Development: SETD2 and the Consequences of Lost Methylation

Catherine C Fahey1, Ian J Davis1,2

  • 1Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7295.

Cold Spring Harbor Perspectives in Medicine
|February 5, 2017
PubMed

Insights

SETD2, a key enzyme for histone trimethylation, is frequently mutated in human cancers. Its loss impacts RNA splicing, DNA repair, and methylation, presenting potential therapeutic vulnerabilities.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • The SETD2 enzyme is responsible for H3K36 trimethylation, a crucial epigenetic modification.
  • SETD2 mutations are prevalent in various human cancers, affecting gene transcription.
  • While SETD2 is the sole trimethylase, its precise role in cancer development requires further elucidation.

Purpose of the Study:

  • To investigate the functions of SETD2-mediated H3K36 trimethylation.
  • To understand the downstream effects of SETD2 loss in cancer.
  • To identify potential therapeutic strategies based on SETD2 vulnerabilities.

Main Methods:

  • Analysis of SETD2's association with RNA polymerase.
  • Investigation of SETD2's role in chromatin regulation.
  • Assessment of effector proteins binding to trimethylated H3K36.

Main Results:

  • SETD2 modifies histones at actively transcribed genes via association with RNA polymerase.
  • SETD2-mediated H3K36 trimethylation regulates RNA splicing, DNA damage repair, and DNA methylation.
  • Loss of SETD2 function disrupts these critical cellular processes.

Conclusions:

  • SETD2 plays a vital role in maintaining genomic stability and regulating gene expression.
  • Understanding the consequences of SETD2 loss is crucial for cancer therapy development.
  • Targeting vulnerabilities arising from SETD2 mutations may offer novel therapeutic avenues.

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