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Invasive Cell Fate Requires G1 Cell-Cycle Arrest and Histone Deacetylase-Mediated Changes in Gene Expression

David Q Matus1, Lauren L Lohmer2, Laura C Kelley2

  • 1Department of Biology, Duke University, Box 90338, Durham, NC 27708, USA; Department of Biochemistry and Cell Biology, Stony Brook University, Stony Brook, NY 11794-5215, USA.

Developmental Cell
|October 28, 2015
PubMed

Insights

Cellular invasion, crucial for development and cancer, requires G1 cell-cycle arrest. This study reveals that the nuclear receptor NHR-67 regulates this arrest, impacting invasion and invadopodia formation, offering new therapeutic targets.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Cancer Biology

Background:

  • Mechanisms of invasive cellular behavior are poorly understood, despite their roles in development and cancer.
  • Cellular invasion is a complex process involving specific molecular programs.

Purpose of the Study:

  • To identify factors regulating invasive cellular behavior.
  • To elucidate the role of cell-cycle regulation in cellular invasion.
  • To understand the molecular basis of anchor cell (AC) invasion in Caenorhabditis elegans.

Main Methods:

  • Conducted a screen of transcription factors in Caenorhabditis elegans.
  • Utilized genetic analysis to study the function of the nuclear receptor nhr-67.
  • Investigated the regulation of G1 cell-cycle arrest and its impact on invasion-related gene expression and invadopodia formation.

Main Results:

  • Identified G1 cell-cycle arrest as a requirement for the AC invasion program.
  • NHR-67 regulates G1 arrest, partly via the cyclin-dependent kinase inhibitor cki-1.
  • Loss of nhr-67 leads to non-invasive, mitotic ACs lacking invadopodia and key invasion-related gene expression.
  • G1 arrest is essential for HDA-1 to promote pro-invasive gene expression and invadopodia formation.

Conclusions:

  • Invasive cell fate necessitates G1 cell-cycle arrest.
  • Targeting both G1-arrested and actively cycling cells may be a strategy to inhibit metastatic cancer.
  • NHR-67 and HDA-1 are key regulators of the invasive cellular program.

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