Key result
Strongly metastatic carcinoma cells express voltage-gated Na+ channels and reduced K+ currents, generating action potentials that support the cellular excitability hypothesis of metastasis.
Proposes the CELEX hypothesis, suggesting that metastatic carcinoma cells acquire cellular excitability through voltage-gated ion channels.
Supports CELEX hypothesis in metastasis; hypothesis-generating and should not change practice without validation.
Biophysics of Cancer: Cellular Excitability (“CELEX”) Hypothesis of Metastasis This article advances a novel hypothesis of metastasis called “CELEX” (for cellular excitability) and presents the current evidence for it. The CELEX hypothesis is based upon concerted expression of voltage-gated ion, particularly Na+ and K+, channels during cancer progression. Electrophysiological recordings from human carcinoma cell lines have shown that, unlike weakly/nonmetastatic cells, cells that have strong metastatic potential express voltage-gated Na+ channels and much reduced outward, mainly K+ currents. Furthermore, the Na+ channel expression is selfsustaining by activity-dependent positive feedback. Thus, strongly metastatic carcinoma cells are excitable and, indeed, generate all-or-none type action potentials, despite their epithelial origin.
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Mustafa B.A. Djamgoz (2014) conducted a review in Cancer metastasis. Voltage-gated Na+ and K+ channels vs. Weakly/nonmetastatic cells was evaluated on Metastatic potential and cellular excitability. Strongly metastatic carcinoma cells express voltage-gated Na+ channels and reduced K+ currents, generating action potentials that support the cellular excitability hypothesis of metastasis.
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