Wnts control membrane potential in mammalian cancer cells

Ashmore, Jonathan; Olsen, Henrik Baare; Sørensen, Naja Møller M.; Thrasivoulou, Christopher; Ahmed, Aamir

doi:10.1113/jp278661

Cited by 12 publications

(11 citation statements)

References 44 publications

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“…The SOCE in turn triggers calcium-dependent potassium channels (KCNN4) leading to a large membrane hyperpolarization. This study indeed suggests that control of membrane potential by Wnt ligands is an early event of the Wnt signaling pathway (Ashmore et al, 2019).…”

Section: Trpm8supporting

confidence: 58%

Interplay Between Ion Channels and the Wnt/β-Catenin Signaling Pathway in Cancers

et al. 2020

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Increasing evidence point out the important roles of ion channels in the physiopathology of cancers, so that these proteins are now considered as potential new therapeutic targets and biomarkers in this disease. Indeed, ion channels have been largely described to participate in many hallmarks of cancers such as migration, invasion, proliferation, angiogenesis, and resistance to apoptosis. At the molecular level, the development of cancers is characterised by alterations in transduction pathways that control cell behaviors. However, the interactions between ion channels and cancer-related signaling pathways are poorly understood so far. Nevertheless, a limited number of reports have recently addressed this important issue, especially regarding the interaction between ion channels and one of the main driving forces for cancer development: the Wnt/b-catenin signaling pathway. In this review, we propose to explore and discuss the current knowledge regarding the interplay between ion channels and the Wnt/b-catenin signaling pathway in cancers.

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Section: Trpm8supporting

confidence: 58%

Interplay Between Ion Channels and the Wnt/β-Catenin Signaling Pathway in Cancers

et al. 2020

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“…The consequence of this difference is that the resting V m needed to reach both the first and second thresholds is lower in cancer cells than in non-cancer cells. The relatively depolarized resting V m in cancer cells [ 28 , 29 , 30 , 31 , 73 , 74 , 75 ] could explain why, compared to non-cancer cells, cancer cells are more vulnerable to both electroporation and TTFields [ 67 , 69 ] (see Table S4 ). Table 4 compares the parameters between TTFields and electroporation (DC and AC).…”

Section: Results: Explanatory Modelsmentioning

confidence: 99%

Permeabilizing Cell Membranes with Electric Fields

Aguilar

Chang

et al. 2021

Cancers

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The biological impact of exogenous, alternating electric fields (AEFs) and direct-current electric fields has a long history of study, ranging from effects on embryonic development to influences on wound healing. In this article, we focus on the application of electric fields for the treatment of cancers. In particular, we outline the clinical impact of tumor treating fields (TTFields), a form of AEFs, on the treatment of cancers such as glioblastoma and mesothelioma. We provide an overview of the standard mechanism of action of TTFields, namely, the capability for AEFs (e.g., TTFields) to disrupt the formation and segregation of the mitotic spindle in actively dividing cells. Though this standard mechanism explains a large part of TTFields’ action, it is by no means complete. The standard theory does not account for exogenously applied AEFs’ influence directly upon DNA nor upon their capacity to alter the functionality and permeability of cancer cell membranes. This review summarizes the current literature to provide a more comprehensive understanding of AEFs’ actions on cell membranes. It gives an overview of three mechanistic models that may explain the more recent observations into AEFs’ effects: the voltage-gated ion channel, bioelectrorheological, and electroporation models. Inconsistencies were noted in both effective frequency range and field strength between TTFields versus all three proposed models. We addressed these discrepancies through theoretical investigations into the inhomogeneities of electric fields on cellular membranes as a function of disease state, external microenvironment, and tissue or cellular organization. Lastly, future experimental strategies to validate these findings are outlined. Clinical benefits are inevitably forthcoming.

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“…A study targeting substantia nigra pars reticularis (an area that participates in seizure activity) and ketone bodies observed reduction in neural excitability through K ATP channels and GABA. Ketone bodies keep K ATP channels open, which might increase the expression of the GABA B subunit (157).…”

Section: Mechanisms Of Action Of the Ketogenic Diet And The Participamentioning

confidence: 99%

“…An extracellular increase of K + prevents the release of Ca 2+ , inhibiting the signaling of the Wnt pathway and the translocation of β-catenin to the cell nucleus. Wnt ligands hyperpolarized the cells by activating K + current by Ca 2+ (157). The Wnt response also depends on the activation of Bcl9 that activates genes that have response sequences to Wnt (158,159).…”

Section: Mechanisms Of Action Of the Ketogenic Diet And The Participamentioning

confidence: 99%

Caloric Restriction and Ketogenic Diet Therapy for Epilepsy: A Molecular Approach Involving Wnt Pathway and KATP Channels

et al. 2020

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Epilepsy is a neurological disorder in which, in many cases, there is poor pharmacological control of seizures. Nevertheless, it may respond beneficially to alternative treatments such as dietary therapy, like the ketogenic diet or caloric restriction. One of the mechanisms of these diets is to produce a hyperpolarization mediated by the adenosine triphosphate (ATP)-sensitive potassium (K ATP) channels (K ATP channels). An extracellular increase of K + prevents the release of Ca 2+ by inhibiting the signaling of the Wnt pathway and the translocation of β-catenin to the cell nucleus. Wnt ligands hyperpolarize the cells by activating K + current by Ca 2+. Each of the diets described in this paper has in common a lower use of carbohydrates, which leads to biochemical, genetic processes presumed to be involved in the reduction of epileptic seizures. Currently, there is not much information about the genetic processes implicated as well as the possible beneficial effects of diet therapy on epilepsy. In this review, we aim to describe some of the possible genes involved in Wnt pathways, their regulation through the K ATP channels which are implicated in each one of the diets, and how they can reduce epileptic seizures at the molecular level.

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Wnts control membrane potential in mammalian cancer cells

Cited by 12 publications

References 44 publications

Interplay Between Ion Channels and the Wnt/β-Catenin Signaling Pathway in Cancers

Interplay Between Ion Channels and the Wnt/β-Catenin Signaling Pathway in Cancers

Permeabilizing Cell Membranes with Electric Fields

Caloric Restriction and Ketogenic Diet Therapy for Epilepsy: A Molecular Approach Involving Wnt Pathway and KATP Channels

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