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Cell fate determination factor DACH1 inhibits c-Jun-induced contact-independent growth

Kongming Wu1, Manran Liu, Anping Li

  • 1Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.

Molecular Biology of the Cell
|December 22, 2006
PubMed

Insights

DACH1 inhibits c-Jun-induced cell proliferation by repressing the c-Jun delta domain. This mechanism involves histone deacetylase recruitment, blocking AP-1 transcriptional activity and contact-independent growth.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • DACH1 is a cell fate determination factor involved in differentiation.
  • DACH1 functions in various transcriptional complexes.
  • c-Jun is a component of AP-1 transcription factor, promoting cell growth.

Purpose of the Study:

  • Investigate DACH1's role in regulating c-Jun activity.
  • Elucidate the mechanism by which DACH1 inhibits c-Jun-induced proliferation.
  • Determine the specific domains involved in DACH1-mediated repression.

Main Methods:

  • Utilized Cre-lox system for c-Jun excision in 3T3 cells.
  • Assessed DNA synthesis and cellular proliferation.
  • Performed co-precipitation assays to identify interacting proteins.
  • Analyzed transcriptional activity of c-Jun and its target genes.

Main Results:

  • DACH1 inhibited c-Jun-induced DNA synthesis and proliferation.
  • DACH1 repressed c-Jun and c-fos transcription via its N-terminal domain.
  • DACH1 repressed c-Jun transactivation through its delta domain, involving HDACs.
  • v-Jun lacking the delta domain was resistant to DACH1 repression.

Conclusions:

  • DACH1 inhibits c-Jun-mediated contact-independent growth.
  • DACH1 represses c-Jun activity by targeting the delta domain.
  • Histone deacetylase recruitment is a key mechanism in DACH1-mediated repression of c-Jun.

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