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Data on the negative regulation of invadopodia activity by MLCK

Rachel J Jerrell1, Aron Parekh1,2,3

  • 1Department of Otolaryngology, Vanderbilt University Medical Center, US.

Data in Brief
|May 22, 2019
PubMed

Insights

Inhibiting myosin light chain kinase (MLCK) in cancer cells unexpectedly increased extracellular matrix (ECM) degradation and invadopodia formation. This suggests a complex role for MLCK in cancer cell invasion and ECM remodeling.

Area of Science:

  • Cancer Biology
  • Cellular Mechanics
  • Extracellular Matrix Dynamics

Background:

  • Actomyosin contractility drives extracellular matrix (ECM) degradation via invadopodia in cancer cells.
  • Previous studies indicated that inhibiting myosin light chain kinase (MLCK) did not alter force generation in head and neck squamous cell carcinoma (HNSCC) cells.

Purpose of the Study:

  • To investigate the effect of targeted myosin light chain kinase (MLCK) knockdown on extracellular matrix (ECM) degradation and invadopodia activity in HNSCC cells.
  • To clarify the role of MLCK in regulating cancer cell invasion mechanisms.

Main Methods:

  • Utilized siRNA to achieve targeted knockdown (KD) of myosin light chain kinase (MLCK) in the SCC-61 HNSCC cell line.
  • Quantified extracellular matrix (ECM) degradation, the number of actively degrading invadopodia, and the total number of invadopodia formed.

Main Results:

  • MLCK knockdown (KD) significantly increased the amount of ECM degradation.
  • A significant increase in the number of actively degrading invadopodia was observed post-MLCK KD.
  • The total number of invadopodia formed also significantly increased following MLCK KD.

Conclusions:

  • Targeted inhibition of MLCK unexpectedly enhances ECM degradation and invadopodia formation in HNSCC cells.
  • These findings suggest that MLCK may play an inhibitory role in cancer cell invasion, contrary to previous assumptions about its role in force generation.
Keywords:
CancerContractilityInvadopodiaInvasionMLCK

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