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Gleevec, an Abl family inhibitor, produces a profound change in cell shape and migration

Zaozao Chen1, Elizabeth Lessey, Matthew E Berginski

  • 1Department of Cell Biology and Physiology, University of North Carolina School of Medicine, Chapel Hill, North Carolina, United States of America.

Plos One
|January 10, 2013
PubMed

Insights

Gleevec (Imatinib) treatment dramatically alters rat bladder tumor cell shape and migration by increasing cell-adhesion strength and traction force. This kinase inhibitor promotes cell spreading and faster, more persistent migration on collagen.

Area of Science:

  • Cell Biology
  • Biophysics
  • Pharmacology

Background:

  • The relationship between cell contractility, adhesion, shape, and migration is complex and not fully understood.
  • Investigating how pharmacological agents impact these fundamental cellular processes is crucial for understanding cell behavior.

Purpose of the Study:

  • To investigate the effects of Gleevec (Imatinib), an Abl family kinase inhibitor, on the morphology and migration of rat bladder tumor cells (NBTII).
  • To elucidate the underlying mechanisms involving cell adhesion, contractility, and RhoA activity.

Main Methods:

  • Treatment of NBTII cells with Gleevec on collagen-coated substrates.
  • Analysis of cell shape and migration patterns.
  • Assessment of integrin-mediated adhesion using total internal reflection fluorescence microscopy (TIRFM) and interference reflection microscopy (IRM).
  • Measurement of cell-substrate adhesion strength via laminar flow experiments.
  • Quantification of RhoA activity and traction force.

Main Results:

  • Gleevec induced a D-shaped morphology and increased migration speed and persistence.
  • Cells exhibited enhanced integrin-mediated adhesion with increased size and number of adhesions, including a dynamic band near the leading edge.
  • Global cell-substrate adhesion strength and total traction force significantly increased.
  • RhoA activity and myosin activation were elevated in Gleevec-treated cells.

Conclusions:

  • Gleevec (Imatinib) profoundly alters NBTII cell morphology and migration by enhancing cell-substrate adhesion and contractility.
  • Increased RhoA activity and myosin-dependent force generation contribute to the observed changes in cell shape and migration.
  • These findings provide insights into the regulation of cell migration by kinase inhibitors.

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