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Genome-wide CRISPR screening identifies a role for ARRDC3 in TRP53-mediated responses

John E La Marca1,2,3,4, Brandon J Aubrey1,2,5, Bruce Yang1,2

  • 1The Walter and Eliza Hall Institute, Parkville, Victoria, Australia.

Cell Death and Differentiation
|December 14, 2023
PubMed

Insights

The tumor suppressor TRP53 normally inhibits tumor growth. We found that ARRDC3 loss enhances MYC-driven lymphoma survival, revealing ARRDC3 as a key TRP53-regulated tumor suppressor.

Area of Science:

  • Genomics
  • Cancer Biology
  • Molecular Oncology

Background:

  • Whole-genome CRISPR screens are vital for identifying novel tumor suppressors and factors influencing anti-cancer agent responses.
  • The tumor suppressor TRP53 plays a critical role in regulating cell fate and tumor suppression.

Purpose of the Study:

  • To identify novel inhibitors of tumor expansion induced by the tumor suppressor TRP53 in lymphoma cells.
  • To investigate the role of Arrestin domain containing 3 (ARRDC3) in MYC-driven lymphoma.

Main Methods:

  • Genome-wide CRISPR screening in lymphoma cells.
  • In vivo studies involving Arrdc3 deletion in mice.
  • Analysis of MYC-driven lymphoma development and response to TRP53-activating anti-cancer agents.

Main Results:

  • Absence of ARRDC3 promotes survival and competitiveness of MYC-driven lymphoma cells under TRP53-activating anti-cancer therapy.
  • Arrdc3 deletion in mice leads to perinatal lethality with developmental abnormalities, including cardiac defects.
  • Loss of ARRDC3 accelerates MYC-driven lymphoma development.

Conclusions:

  • ARRDC3 is a novel mediator of TRP53-induced tumor suppression.
  • Targeting ARRDC3 may offer new therapeutic strategies for MYC-driven lymphomas and other cancers.
  • Understanding ARRDC3's role in development and cancer is crucial for future therapeutic applications.

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