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Cytoskeleton and nucleotide signaling in glioma C6 cells

Wanda Kłopocka1, Jarosław Korczyński, Paweł Pomorski

  • 1Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur St, PL 02-093, Warsaw, Poland. w.klopocka@nencki.gov.pl

Advances in Experimental Medicine and Biology
|August 11, 2012
PubMed

Insights

The P2Y(2) nucleotide receptor (P2Y(2)R) in glioma cells regulates actin cytoskeleton dynamics. UTP stimulation of P2Y(2)R reverses RhoA/ROCK pathway inhibition, restoring cell shape and actin organization via calcium signaling and Rac1 activation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Neuroscience

Background:

  • Glioma cell migration and morphology are influenced by actin cytoskeleton dynamics.
  • The P2Y(2) nucleotide receptor (P2Y(2)R) is implicated in cellular signaling.
  • Actin cytoskeleton regulation is crucial for cell shape, migration, and focal adhesion formation.

Purpose of the Study:

  • To elucidate the signaling pathways regulated by the P2Y(2)R in glioma C6 cells.
  • To investigate the role of P2Y(2)R in modulating actin cytoskeleton dynamics.
  • To understand the interplay between P2Y(2)R, RhoA/ROCK, and Rac1 pathways in glioma cell behavior.

Main Methods:

  • Utilized glioma C6 cells to study P2Y(2)R signaling.
  • Investigated the effects of ATP and UTP on cellular processes.
  • Employed Rho-kinase inhibitors to block the RhoA/ROCK pathway.
  • Analyzed changes in F-actin organization, cell shape, and protein phosphorylation (myosin II, cofilin).
  • Examined the involvement of calcium signaling and Rac1 activation.

Main Results:

  • P2Y(2)R activation by nucleotides modulates phosphatidylinositol-4,5-bisphosphate (PIP(2)) levels, affecting actin binding proteins.
  • The RhoA/ROCK pathway is crucial for stress fiber assembly and cell migration; its inhibition alters F-actin organization and cell shape.
  • UTP stimulation of P2Y(2)R in glioma cells reverses RhoA/ROCK inhibition-induced changes, involving calcium signaling.
  • Rac1 activation, dependent on G(o) proteins, α(v)β(5) integrins, and P2Y(2)Rs, is essential for cofilin phosphorylation and lamellipodium stabilization.
  • Inhibition of positive Rac1 regulation prevents the recovery of normal cell morphology in glioma cells.

Conclusions:

  • The P2Y(2)R plays a significant role in regulating actin cytoskeleton dynamics in glioma C6 cells through complex signaling pathways.
  • Cross-talk between RhoA/ROCK, calcium signaling, and Rac1 pathways, modulated by P2Y(2)R and integrins, dictates glioma cell morphology and migration.
  • Targeting P2Y(2)R-mediated signaling offers potential therapeutic strategies for glioma by controlling cell behavior.

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