Roles of K + channels in regulating tumour cell proliferation and apoptosis
Abstract
K+ channels are a most diverse class of ion channels in the cytoplasmic membrane and are distributed widely in a variety of cells including cancer cells. Cell proliferation and apoptosis (programmed cell death or cell suicide) are two counterparts that share the responsibility for maintaining normal tissue homeostasis. Evidence has been accumulating from fundamental studies indicating that tumour cells possess various types of K+ channels, and that these K+ channels play important roles in regulating tumour cell proliferation and apoptosis, i.e. facilitating unlimited growth and promoting apoptotic death of tumour cells. The potential implications of K+ channels as a pharmacological target for cancer therapy and a biomarker for diagnosis of carcinogenesis are attracting increasing interest. This review aims to provide a comprehensive overview of current status of research on K+ channels/currents in tumour cells. Focus is placed on the roles of K+ channels/currents in regulating tumour cell proliferation and apoptosis. The possible mechanisms by which K+ channels affect tumour cell growth and death are discussed. Speculations are also made on the potential implications of regulation of tumour cell proliferation and apoptosis by K+ channels.
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Ion channel-mediated Vm hyperpolarization would increase the electrochemical gradient for Ca2+ and therefore elevate the intracellular Ca2+ concentration through voltage-independent Ca2+ channels, such as transient receptor potential (TRP) channels.
“Alternatively, ion channel-mediated Vm hyperpolarization would increase the electrochemical gradient for Ca2+ and therefore elevate the intracellular Ca2+ concentration through voltage-independent Ca2+ channels, such as transient receptor potential (TRP) channels (Nilius and Wohlrab, 1992; Wang, 2004; Ouadid-Ahidouch and Ahidouch, 2008).”
From Membrane potential and cancer progression (2013) · cites this paper as Wang, 2004
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Blackiston, D. J., McLaughlin, K. A., & Levin, M. (2009) · Cell Cycle · doi:10.4161/cc.8.21.9888 · Cited by 468 · see citing works
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- Authors
- Wang, Z.
- Affiliations
- Montreal Heart Institute (CA)
- Corresponding author
- Wang, Zhiguo
- ORCID
- Wang, Zhiguo
- Venue
- Pfl�gers Archiv European Journal of Physiology
- Published
- 2004-06-01
- Volume
- 448
- Issue
- 3
- Pages
- 274-286
- ISSN
- 0031-6768 (ISSN-L)
- 1432-2013
- OpenAlex
- W2064821447
- Cited by
- 280
- References
- 0
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 10 · 2023: 8 · 2022: 3 · 2021: 8 · 2020: 9 · 2019: 10 · 2018: 7 · 2017: 6 · 2016: 11 · 2015: 11 · 2014: 18 · 2013: 19 · 2012: 14
- FWCI
- 6.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Pflügers Archiv - European Journal of Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Keywords
- potassium channels, tumor cell proliferation, apoptosis, cancer cells, ionic currents, cancer therapy targets, biomarkers of carcinogenesis
- MeSH terms
- Animals, Humans, Membrane Potentials, Neoplasms, Biomarkers, Tumor, Potassium Channels, Apoptosis, Cell Proliferation
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