Cited by 239Connexins and lens biologyIon channel regulation and functionIon Transport and Channel Regulation

Membrane potentials and sodium channels: Hypotheses for growth regulation and cancer formation based on changes in sodium channels and gap junctions

Binggeli, Richard, Weinstein, Roy C.·1986·Journal of Theoretical Biology

Abstract

Based on several convergent lines of investigation, we make two hypotheses which are sufficient to explain many phenomena of growth regulation in both normal and cancer cells. 1. The first hypothesis is that there is a boundary or threshold of resting cell membrane potential that separates normal resting cells from normal proliferating cells and cancer cells. The basis for this in existing literature values of membrane potentials in resting and proliferating cells is established. A discussion of how these differences in potential can be explained focuses on changes in sodium permeability and internal sodium concentration. Of many sodium transfer mechanisms, the sodium channel is emphasized and how increased intracellular transfer may stimulate DNA synthesis. The effects of changing cell junctions, in particular gap junctions, on membrane potentials is also discussed, as well as the indications of altered junctions in tumor cells. The linking factor of the effects of growth factors on both cell junctions and sodium permeability leads to the second hypothesis. 2. Since growth initiation and inhibition involve sodium channels and gap junctions, several phenomena can be explained by postulating that they are one and the same entity. The basis for this hypothesis in existing descriptions of functional and structural similarities is outlined. The possible interchange of these elements in the cell cycle lead to several corollaries consequent to the conservation of their total number…

Integrity signals

Registry

Crossref · 10.1016/s0022-5193(86)80209-0

Cites

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Proliferative cells, especially rapidly proliferating tumor cells, displayed depolarized Vm, whereas non-proliferating, terminally differentiated somatic cells, such as muscle cells and neurons, are characterized by their hyperpolarized Vm.

    “Recordings from rodent and human tissues have revealed that proliferative cells, especially rapidly proliferating tumor cells, displayed depolarized Vm, whereas non-proliferating, terminally differentiated somatic cells, such as muscle cells and neurons, are characterized by their hyperpolarized Vm (Figure 1) [reviewed in Binggeli and Weinstein (1986)].”

    From Membrane potential and cancer progression (2013) · cites this paper as Binggeli and Weinstein, 1986

  • Changes in Vm control critical cell functions including proliferation, migration, and differentiation.

    “Since then, changes in Vm, representing the long-term, slowly changing bioelectric gradient in non-excitable cells (Lobikin et al., 2012), have been shown to control critical cell functions including proliferation, migration, and differentiation (Binggeli and Weinstein, 1986; Schwab et al., 2007; Blackiston et al., 2009; Sundelacruz et al., 2009).”

    From Membrane potential and cancer progression (2013) · cites this paper as Binggeli and Weinstein, 1986

  • In both highly proliferative tumor and non-tumor cells, depolarization is believed to serve as a signal that could initiate mitosis and DNA synthesis.

    “In general, in both highly proliferative tumor and non-tumor cells, depolarization is believed to serve as a signal that could initiate mitosis and DNA synthesis (Orr et al., 1972; Binggeli and Weinstein, 1986).”

    From Membrane potential and cancer progression (2013) · cites this paper as Binggeli and Weinstein, 1986

  • Vm modulates important cellular activities, such as proliferation and differentiation.

    “changes in Vm, representing the long-term, slowly changing bioelectric gradient in non-excitable cells (Lobikin et al., 2012), have been shown to control critical cell functions including proliferation, migration, and differentiation (Binggeli and Weinstein, 1986; Schwab et al., 2007; Blackiston et al., 2009; Sundelacruz et al., 2009).”

    From Membrane potential and cancer progression (2013) · cites this paper as Binggeli and Weinstein, 1986

Cited by

Sorted by citations

Authors
Binggeli, R., & Weinstein, R. C.
Affiliations
University of Southern California (US)
Venue
Journal of Theoretical Biology
Publisher
Elsevier BV
Published
1986-12
Volume
123
Issue
4
Pages
377-401
ISSN
0022-5193 (ISSN-L)
OpenAlex
W2022003983
Cited by
239
References
0
Citations by year
2026: 7 · 2025: 12 · 2024: 18 · 2023: 10 · 2022: 9 · 2021: 8 · 2020: 12 · 2019: 6 · 2018: 12 · 2017: 10 · 2016: 13 · 2015: 13 · 2014: 19 · 2013: 5 · 2012: 9
FWCI
0.86
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Theoretical Biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connexins and lens biology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
membrane potential, sodium channels, gap junctions, cell growth regulation, carcinogenesis, sodium permeability, intracellular sodium concentration, DNA synthesis, cell junctions, growth factors, cell cycle, connexons, cancer cells
MeSH terms
Cell Cycle, Cell Division, Cell Transformation, Neoplastic, DNA, Intercellular Junctions, Ion Channels, Membrane Potentials, Sodium

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review