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Global changes in chromatin accessibility and transcription following ATRX inactivation in human cancer cells

Junbo Liang1, Hongchao Liu1, Guangyu Li1

  • 1State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.

FEBS Letters
|July 23, 2019
PubMed

Insights

Loss of alpha-thalassemia mental retardation X-linked (ATRX) causes widespread epigenomic changes in cancer cells, affecting repetitive DNA and regulatory regions. ATRX deficiency promotes tumorigenesis via genome instability and altered gene transcription.

Area of Science:

  • Cancer Biology
  • Epigenetics
  • Chromatin Remodeling

Background:

  • Alpha-thalassemia mental retardation X-linked (ATRX) is a chromatin remodeler frequently mutated in various cancers.
  • While ATRX binds to heterochromatin, its specific epigenomic impact, particularly in these regions, remains largely uncharacterized in cancer cells.

Purpose of the Study:

  • To profile genome-wide chromatin accessibility changes in human cancer cells with and without ATRX.
  • To investigate the epigenomic consequences of ATRX loss, focusing on heterochromatin and regulatory elements.

Main Methods:

  • Genome-wide chromatin accessibility mapping (e.g., ATAC-seq or similar) was performed on isogenic ATRX-intact and ATRX-null human cancer cell lines.
  • Analysis correlated changes in chromatin accessibility with gene expression data.

Main Results:

  • ATRX loss led to extensive alterations in chromatin accessibility across both repetitive DNA and non-repetitive regulatory regions.
  • These accessibility changes were strongly correlated with significant shifts in gene transcription.
  • Key cancer-related signaling pathways were affected, including upregulation of TGF-β signaling and downregulation of cadherin proteins.

Conclusions:

  • ATRX deficiency induces substantial epigenomic alterations in cancer cells.
  • These ATRX-mediated changes contribute to tumorigenesis by promoting genome instability and altering transcriptional programs, impacting critical cancer pathways.
Keywords:
ATRXATAC-seqTGF-βheterochromatin

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