Key result
Tetrodotoxin or SCN8A knockdown inhibits macrophage and melanoma cell invasion by blocking NaV1.6-driven podosome formation.
Why the study?
The role of a splice variant of the sodium channel SCN8A in regulating podosome and invadopodia formation and cellular invasion in macrophages and melanoma cells was not established.
Population
THP-1 human monocyte-macrophage cells, mouse peritoneal macrophages, HTB-66 invasive melanoma cells
Comparison
Pharmacologic antagonism with tetrodotoxin, agonist activation with veratridine, and SCN8A knockdown vs control
Design
Preclinical cellular and molecular study
Authors
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Animal data on NaV1.6 should not change practice; leaves open human relevance and therapeutic targeting of invasion.
A splice variant of the sodium channel NaV1.6 regulates podosome formation and cellular invasion in macrophages and melanoma cells, suggesting a novel role for intracellular sodium release in these processes.
Carrithers et al. (2009) studied this question. Tetrodotoxin (TTX) or SCN8A knockdown was evaluated on Podosome formation and cellular invasion. A splice variant of NaV1.6 regulates cellular invasion through podosome and invadopodia formation in macrophages and melanoma cells, which is inhibited by tetrodotoxin or SCN8A knockdown.
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