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The Tumor Suppressor ARID1A Controls Global Transcription via Pausing of RNA Polymerase II

Marco Trizzino1, Elisa Barbieri1, Ana Petracovici2

  • 1The Wistar Institute, Gene Expression and Regulation Program, 3601 Spruce Street, Philadelphia, PA 19104, USA.

Cell Reports
|June 28, 2018
PubMed

Insights

Loss of ARID1A in ovarian cancer impairs RNA polymerase II pausing, disrupting gene transcription. Upregulation of ARID1B can compensate, but some critical genes remain dysregulated, offering insights into ARID1A-driven tumorigenesis.

Area of Science:

  • Cancer Biology
  • Epigenetics
  • Molecular Oncology

Background:

  • ARID1A and ARID1B are subunits of the SWI/SNF chromatin remodeler.
  • ARID1A mutations are frequent in cancers, especially ovarian clear cell carcinoma (OCCC).
  • The precise role of ARID1A in tumorigenesis is not fully understood.

Purpose of the Study:

  • To investigate the functional mechanism of ARID1A in OCCC.
  • To elucidate how ARID1A loss impacts transcription and chromatin regulation.
  • To identify ARID1A-dependent genes and their regulation.

Main Methods:

  • Depletion of ARID1A in OCCC cells.
  • Analysis of RNA polymerase II (RNAPII) transcription and chromatin accessibility.
  • Quantitative assessment of gene expression changes.

Main Results:

  • ARID1A binds to active regulatory elements in OCCC.
  • ARID1A depletion represses RNAPII transcription and severely impairs RNAPII pausing.
  • ARID1B upregulation compensates for some ARID1A loss, but not for all ARID1A-dependent genes, including p53 and ESR1 targets.

Conclusions:

  • ARID1A plays a critical role in regulating RNAPII dynamics and transcription in OCCC.
  • Dysregulation of ARID1A-dependent genes contributes to OCCC tumorigenesis.
  • SWI/SNF's function in modulating RNAPII dynamics is highlighted.
Keywords:
ARID1AARID1BRNAPIISWI/SNFovarian clear cell carcinomapausingtranscription

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