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Myocardin inhibits cellular proliferation by inhibiting NF-kappaB(p65)-dependent cell cycle progression

Ru-Hang Tang1, Xi-Long Zheng, Thomas E Callis

  • 1Departments of Surgery and Cell and Developmental Biology, Carolina Cardiovascular Biology Center, and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.

Proceedings of the National Academy of Sciences of the United States of America
|February 26, 2008
PubMed

Insights

Myocardin, a protein regulating muscle genes, was found to inhibit cell proliferation by interacting with NF-kappaB. This interaction reveals a new role for myocardin in controlling cell growth and differentiation.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Genetics

Background:

  • Myocardin is crucial for muscle gene expression and its inactivation is linked to tumor growth.
  • The precise mechanism of myocardin's regulation of cellular growth is not fully understood.
  • NF-kappaB is a key inflammatory transcription factor involved in cellular fate determination.

Purpose of the Study:

  • To elucidate the mechanism by which myocardin regulates cellular growth.
  • To investigate the functional interaction between NF-kappaB and myocardin.
  • To determine myocardin's role in cellular proliferation and differentiation.

Main Methods:

  • Investigated the interaction between NF-kappaB(p65) and myocardin.
  • Analyzed the effect of NF-kappaB on myocardin's activation of muscle genes.
  • Assessed myocardin's impact on NF-kappaB-mediated gene expression and cell-cycle regulation.
  • Utilized in vitro and in vivo assays to study complex formation and DNA binding.

Main Results:

  • NF-kappaB(p65) represses myocardin's activation of cardiac and smooth muscle genes.
  • p65 directly interacts with myocardin, inhibiting the myocardin/SRF/CArG complex formation.
  • Myocardin inhibits p65-mediated gene activation and abrogates LPS-induced TNF-alpha expression.
  • Myocardin inhibits cellular proliferation via interference with NF-kappaB-dependent cell-cycle regulation.

Conclusions:

  • Myocardin functions as an SRF-independent transcriptional repressor and cell-cycle regulator.
  • The interaction between NF-kappaB and myocardin is central to modulating cellular proliferation and differentiation.
  • This study provides a molecular mechanism for myocardin's role in cellular growth control.

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