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Dissection of HEF1-dependent functions in motility and transcriptional regulation

Sarah J Fashena1, Margret B Einarson, Geraldine M O'Neill

  • 1Fox Chase Cancer Center, 7701 Burholme Ave, Philadelphia, PA 19111, USA.

Journal of Cell Science
|January 22, 2002
PubMed

Insights

The study reveals how Human Enhancer of Filamin (HEF1) protein regulates cell movement and morphology. Increased HEF1 levels enhance cell motility and influence genes linked to cancer progression.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cas-family proteins are crucial signaling intermediates in cellular processes like attachment, motility, and oncogenic transformation.
  • The three Cas-family members (p130Cas, HEF1/Cas-L, Efs/Sin) have complex regulation, making specific function elucidation challenging.

Purpose of the Study:

  • To investigate the biological role of Human Enhancer of Filamin (HEF1) using a novel inducible system.
  • To understand how regulated HEF1 production impacts cellular behavior and gene expression.

Main Methods:

  • Development of cell lines with inducible HEF1 production.
  • Analysis of cellular morphology and motility changes.
  • cDNA expression array analysis to identify affected gene transcripts.
  • Investigation of involvement of ERK and p38 MAPK signaling pathways.

Main Results:

  • Inducible HEF1 production rapidly altered cell morphology and enhanced cell motility and haptotaxis towards fibronectin.
  • These motility changes were partially dependent on intact ERK and p38 MAPK signaling pathways.
  • HEF1 production upregulated mRNA transcripts for proteins associated with motility, cell transformation, and invasiveness, including metalloproteinases, MLCK, p160ROCK, and ErbB2.

Conclusions:

  • Regulated HEF1 production significantly impacts cell motility and morphology.
  • Upregulation of specific genes by HEF1 suggests potential mechanisms for its role in cancer progression.
  • Misregulation of HEF1 may contribute to cancer development through altered expression of motility and invasiveness-associated proteins.

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