Cited by 78Ion channel regulation and functionIon Channels and ReceptorsCalcium signaling and nucleotide metabolism

KCa2.3 channel-dependent hyperpolarization increases melanoma cell motility

Chantome, Aurelie, Girault, Alban, Potier, Marie, Collin, Christine, Vaudin, Pascal, Pagès, Jean-Christophe, Vandier, Christophe, Joulin, Virginie·2009·Experimental Cell Research

Abstract

Cell migration and invasion are required for tumour cells to spread from the primary tumour bed so as to form secondary tumours at distant sites. We report evidence of an unusual expression of KCa2.3 (SK3) protein in melanoma cell lines but not in normal melanocytes. Knockdown of the KCa2.3 channel led to plasma membrane depolarization, decreased 2D and 3D cell motility. Conversely, enforced production of KCa2.3 protein in KCa2.3 non-expressing cells led to the plasma membrane becoming hyperpolarized, and enhanced cell motility. In contrast, KCa3.1 channels had no effect on cell motility despite an active role in regulating membrane potential. Our data also suggest that membrane hyperpolarization increases melanoma cell motility and that this occurs through the KCa2.3 channel. Our findings reveal a previously unknown function of the KCa2.3 channel, and suggest that the KCa2.3 channel might be the only member of the Ca(2+)-activated K(+) channel family involved in melanoma cell motility pathways.

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Crossref · 10.1016/j.yexcr.2009.07.021

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  • In several breast carcinoma/melanoma cell lines, KCa2.3, which is responsible for maintaining a hyperpolarized Vm, enhances migration, likely via promotion of intracellular Ca2+ signaling.

    “In several breast carcinoma/melanoma cell lines, KCa2.3, which is responsible for maintaining a hyperpolarized Vm, enhances migration, likely via promotion of intracellular Ca2+ signaling (Potier et al., 2006; Chantome et al., 2009).”

    From Membrane potential and cancer progression (2013) · cites this paper as Chantome et al., 2009

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Authors
Chantome, A., Girault, A., Potier, M., Collin, C., Vaudin, P., Pagès, J.-C., Vandier, C., & Joulin, V.
Affiliations
  • Université de Tours (FR)
  • Centre National de la Recherche Scientifique (FR)
Corresponding author
Vandier, Christophe
Venue
Experimental Cell Research
Publisher
Elsevier BV
Published
2009-12
Volume
315
Issue
20
Pages
3620-3630
ISSN
0014-4827 (ISSN-L)
OpenAlex
W2075764726
Cited by
78
References
42
Citations by year
2025: 1 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 5 · 2020: 5 · 2019: 1 · 2018: 8 · 2017: 7 · 2016: 4 · 2015: 3 · 2014: 5 · 2013: 12 · 2012: 8
FWCI
2.42
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Cell Research (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Funders
Ligue Contre le Cancer
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
Keywords
KCa2.3, SK3 channel, melanoma, cell motility, membrane hyperpolarization, plasma membrane depolarization, KCa3.1, calcium-activated potassium channels, tumor invasion, cell migration, membrane potential
MeSH terms
Apamin, Cell Movement, Clotrimazole, Humans, Melanocytes, Melanoma, Membrane Potentials, Pyrazoles, Transfection, Gene Expression, RNA, Antisense, Patch-Clamp Techniques, Potassium Channel Blockers, Cell Line, Tumor, Cell Proliferation, Small-Conductance Calcium-Activated Potassium Channels, Intermediate-Conductance Calcium-Activated Potassium Channels, Electrophysiological Phenomena

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