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Repression of SRF target genes is critical for Myc-dependent apoptosis of epithelial cells

Katrin E Wiese1, Heidi M Haikala2, Björn von Eyss1

  • 1Biocenter Theodor Boveri Institute University of Würzburg, Würzburg, Germany.

The EMBO Journal
|April 22, 2015
PubMed

Insights

High Myc levels trigger cell death by partnering with Miz1, repressing survival genes. Restoring SRF activity counteracts this, preventing Myc-induced apoptosis in epithelial cells.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Oncogenic Myc expression sensitizes cells to apoptosis, preventing cancer.
  • Mechanisms by which cells distinguish physiological from supraphysiological Myc levels are unclear.

Purpose of the Study:

  • To investigate how Myc induces apoptosis in breast epithelial cells.
  • To elucidate the role of Miz1 in Myc-mediated transcriptional repression and apoptosis.

Main Methods:

  • Gene expression analysis
  • Chromatin immunoprecipitation sequencing (ChIP-Seq)
  • Functional assays assessing apoptosis and protein activity

Main Results:

  • Myc induces apoptosis in breast epithelial cells via association with Miz1.
  • High Myc levels, in complex with Miz1, repress transcription of genes involved in cell adhesion and migration, including integrins.
  • Repressed genes are enriched for serum-response factor (SRF) binding sites.
  • Restoring SRF activity antagonizes Myc repression, reduces Myc-induced apoptosis, and reverses decreased Akt phosphorylation.

Conclusions:

  • High Myc levels engage Miz1 to form repressive complexes, suppressing an SRF-dependent survival program in epithelial cells.
  • This mechanism highlights a critical pathway for Myc-induced apoptosis and cancer suppression.
Keywords:
AktMiz1Mycapoptosis

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