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Sphingosine 1-phosphate and human ether-a'-go-go-related gene potassium channels modulate migration in human

Muhammad Yasir Asghar1, Tero Viitanen, Kati Kemppainen

  • 1Department of Biosciences, Åbo Akademi University, Biocity, Turku, Finland.

Endocrine-Related Cancer
|August 15, 2012
PubMed

Insights

Sphingosine 1-phosphate (S1P) inhibits anaplastic thyroid cancer (ATC) cell migration by activating S1P(2) receptors and the Rho pathway. This effect is partly due to a S1P-induced decrease in HERG potassium channel expression.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Pharmacology

Background:

  • Anaplastic thyroid cancer (ATC) is an aggressive thyroid cancer with limited treatment options.
  • Cell migration is a critical process in cancer progression and metastasis.
  • Sphingosine 1-phosphate (S1P) receptors and HERG potassium channels are implicated in modulating cell migration.

Purpose of the Study:

  • To investigate the role of S1P receptors and HERG channels in ATC cell migration.
  • To elucidate the molecular mechanisms underlying S1P-mediated inhibition of ATC cell migration.

Main Methods:

  • Expression analysis of S1P receptors (S1P(1-3)) in human ATC cell lines (C643, THJ-16T) and follicular thyroid cancer cells (FTC-133).
  • Pharmacological inhibition and siRNA-mediated knockdown of S1P receptors (S1P(2)) and Rho pathway components (Rac).
  • Assessment of HERG (KCNH2) potassium channel expression and function in ATC cells and HEK cells overexpressing HERG.
  • Migration assays using pharmacological agents and siRNA to evaluate the effects of S1P, receptor antagonists, and channel modulators.

Main Results:

  • S1P receptors (S1P(1-3)) are expressed in ATC cell lines.
  • S1P inhibited migration of ATC and FTC cells, an effect mediated by S1P(2) receptor activation.
  • S1P-induced inhibition of migration involved the Rho pathway and attenuated Rac activity.
  • S1P decreased HERG protein expression and current in ATC and HERG-overexpressing HEK cells.
  • Downregulation of HERG protein reduced basal cell migration.

Conclusions:

  • S1P attenuates anaplastic thyroid cancer cell migration primarily through S1P(2) receptor activation and the Rho pathway.
  • A S1P-induced decrease in HERG potassium channel expression contributes to the inhibition of ATC cell migration.
  • These findings suggest potential therapeutic targets for managing aggressive thyroid cancer.

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