ArticleCancer cell international2016
Altering bioelectricity on inhibition of human breast cancer cells.
Article in Cancer cell international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 49 citations in OpenAlex.
- Cancer: A bioelectric disease?Clinical and translational medicine · 2026Review
- Network-based exploration of 4-(phenylsulfonyl)morpholine molecules for metastatic triple-negative breast cancer suppression.PLoS computational biology · 2026Article
- Targeting ion channel dysregulation in tumors: emerging therapeutic opportunities.Trends in pharmacological sciences · 2026Review
- Engineering Complex Breast Tumor-Stroma Models: TMPyP4-Photodynamic Therapy Is More Effective at the Metastatic Site in Breast Tumors.ACS biomaterials science & engineering · 2026Article
- Visualizing intracellular milieu and electric field-induced cell responses by fluorescence lifetime imaging microscopy.Scientific reports · 2025Article
- ROS-induced voltage-gated ion channel expression and electrophysiological remodeling in malignant human cells.NPJ systems biology and applications · 2025Article
- Review of electrophysiological models to study membrane potential changes in breast cancer cell transformation and tumor progression.Frontiers in physiology · 2025Review
- Pan-Cancer Screening and Validation of CALU's Role in EMT Regulation and Tumor Microenvironment in Triple-Negative Breast Cancer.Journal of inflammation research · 2024Article
- Nanotechnology and Cancer Bioelectricity: Bridging the Gap Between Biology and Translational Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Impact of REAC Regenerative Endogenous Bioelectrical Cell Reprogramming on MCF7 Breast Cancer Cells.Journal of personalized medicine · 2023Article
- Effects of extremely low frequency electromagnetic fields on the tumor cell inhibition and the possible mechanism.Scientific reports · 2023Article
- Voltage imaging reveals the dynamic electrical signatures of human breast cancer cells.Communications biology · 2022Article
- From HDAC to Voltage-Gated Ion Channels: What's Next? The Long Road of Antiepileptic Drugs Repositioning in Cancer.Cancers · 2022Review
- A Promising Method for the Determination of Cell Viability: The Membrane Potential Cell Viability Assay.Cells · 2022Article
- A computational model of organism development and carcinogenesis resulting from cells' bioelectric properties and communication.Scientific reports · 2022Article
- Histone deacetylase 4 and 5 translocation elicited by microsecond pulsed electric field exposure is mediated by kinase activity.Frontiers in bioengineering and biotechnology · 2022Article
- Bioelectric Dysregulation in Cancer Initiation, Promotion, and Progression.Frontiers in oncology · 2022Review
- Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Quantum Tunneling-Induced Membrane Depolarization Can Explain the Cellular Effects Mediated by Lithium: Mathematical Modeling and Hypothesis.Membranes · 2021Article
- Peptide-based delivery vectors with pre-defined geometrical locks.RSC medicinal chemistry · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMembrane depolarization is associated with breast cancer. Depolarization-activated voltage-gated ion channels are directly implicated in the initiation, proliferation, and metastasis of breast cancer.
methodsIn this study, the role of voltage-gated potassium and calcium ion channel modulation was explored in two different invasive ductal human carcinoma cell lines, MDA-MB-231 (triple-negative) and MCF7 (estrogen-receptor-positive).
resultsResting membrane potential is more depolarized in MCF7 and MDA-MB-231 cells compared to normal human mammary epithelial cells. Increasing extracellular potassium concentration up to 50 mM depolarized membrane potential and greatly increased cell growth. Tetraethylammonium (TEA), a non-specific blocker of voltage-gated potassium channels, stimulated growth of MCF7 cells (control group grew by 201 %, 1 mM TEA group grew 376 %). Depolarization-induced calcium influx was hypothesized as a requirement for growth of human breast cancer. Removing calcium from culture medium stopped growth of MDA and MCF7 cells, leading to cell death after 1 week. Verapamil, a blocker of voltage-gated calcium channels clinically used in treating hypertension and coronary disease, inhibited growth of MDA cells at low concentration (10-20 μM) by 73 and 92 % after 1 and 2 days, respectively. At high concentration (100 μM), verapamil killed >90 % of MDA and MCF7 cells after 1 day. Immunoblotting experiments demonstrated that an increased expression of caspase-3, critical in apoptosis signaling, positively correlated with verapamil concentration in MDA cells. In MCF7, caspase-9 expression is increased in response to verapamil.
conclusionsOur results support our hypotheses that membrane depolarization and depolarization-induced calcium influx stimulate proliferation of human breast cancer cells, independently of cancer subtypes. The underlying mechanism of verapamil-induced cell death involves different caspases in MCF7 and MDA-MB-231. These data suggest that voltage-gated potassium and calcium channels may be putative targets for pharmaceutical remediation in human invasive ductal carcinomas.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.