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Local anesthetics inhibit kinesin motility and microtentacle protrusions in human epithelial and breast tumor cells

Jennifer R Yoon1, Rebecca A Whipple, Eric M Balzer

  • 1Marlene and Stewart Greenebaum Cancer Center, Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Breast Cancer Research and Treatment
|November 12, 2010
PubMed

Insights

Kinesin inhibitors like Tetracaine rapidly collapse microtubule microtentacles (McTNs) on detached breast tumor cells. This reduces tumor cell reattachment and may decrease metastatic progression.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Biophysics

Background:

  • Detached breast tumor cells form microtubule protrusions called microtentacles (McTNs).
  • McTNs are enriched with vimentin and detyrosinated α-tubulin (Glu-tubulin), suggesting kinesin motor protein involvement.
  • Kinesins are implicated in McTN formation and function, potentially influencing cancer metastasis.

Purpose of the Study:

  • To investigate the role of kinesin motor proteins in the formation and function of tubulin microtentacles (McTNs).
  • To evaluate the effects of kinesin inhibitors, Lidocaine and Tetracaine, on McTN dynamics and breast tumor cell behavior.
  • To explore a novel mechanism for how anesthetics might reduce metastatic progression.

Main Methods:

  • Live-cell imaging and McTN counting to observe inhibitor effects.
  • Adhesion assays to measure cell reattachment.
  • Immunofluorescence and video microscopy to visualize McTN collapse and kinesin motility.
  • Viability and apoptosis assays to confirm inhibitor non-toxicity.

Main Results:

  • Lidocaine and Tetracaine treatments rapidly collapsed vimentin filaments in breast tumor cells.
  • Tetracaine reduced intracellular kinesin motility and caused centripetal collapse of McTNs.
  • Tetracaine inhibited McTN extension, tumor cell aggregation, and reattachment, with Lidocaine showing similar but less potent effects.

Conclusions:

  • Kinesin motor protein inhibition by Tetracaine reduces McTN formation and function.
  • This provides a novel mechanism by which Tetracaine may decrease breast cancer metastatic progression.
  • Targeting kinesins offers a potential strategy for anti-metastatic therapies.

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