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Inhibition of cell proliferation by CD44: Akt is inactivated and EGR-1 is down-regulated

L-S Zhang1, H-W Ma, H J Greyner

  • 1Department of Psychiatry and Behavioral Health, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.

Cell Proliferation
|July 2, 2010
PubMed
Abstract

Insights

CD44 protein expression inhibits cell proliferation by inactivating Akt and down-regulating EGR-1. This discovery reveals a novel pathway for CD44 in cell growth regulation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Signal Transduction

Background:

  • CD44 is a transmembrane glycoprotein involved in cell signaling.
  • CD44's role in cell proliferation is complex, with studies suggesting both positive and negative regulation.
  • Understanding CD44's inhibitory mechanisms is crucial for targeted therapies.

Purpose of the Study:

  • To investigate the mechanism by which CD44 inhibits cell proliferation.
  • To elucidate the molecular pathways regulated by CD44 in Jurkat cells.

Main Methods:

  • Engineered Jurkat cells (E6.1) to express CD44, lacking endogenous expression.
  • Utilized RT(2)-PCR array, siRNA, and Western blotting to analyze molecular pathways.
  • Employed pharmacological inhibitors for ERK1/2, p38, and PI3K/Akt pathways.

Main Results:

  • CD44 expression significantly inhibited cell proliferation and down-regulated Early Growth Response 1 (EGR-1) and its targets, cyclin D1 and D2.
  • EGR-1 siRNA transfection also inhibited cell proliferation, confirming its role.
  • Inhibition of the PI3K/Akt pathway mimicked CD44's effects; Akt was hypophosphorylated in CD44-expressing cells.
  • Constitutively active Akt rescued the proliferation defect, highlighting Akt's requirement.

Conclusions:

  • CD44 inactivates Akt, leading to down-regulation of EGR-1.
  • This novel pathway mediated by CD44 inhibits cell proliferation.
  • Findings provide insights into CD44-mediated regulation of cell growth.

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