ArticleBreast cancer research and treatment2007
The neonatal splice variant of Nav1.5 potentiates in vitro invasive behaviour of MDA-MB-231 human breast cancer cells.
Article in Breast cancer research and treatment, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 177 citations in OpenAlex.
- Sodium accumulation in breast cancer predicts malignancy and treatment response.British journal of cancer · 2022Trial
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- Inflammatory Co-Regulation of Voltage-Gated Sodium Channels and Na,K-ATPase in Metastatic Breast Cancer.International journal of molecular sciences · 2025Article
- The local anesthetic, lidocaine, suppresses the growth of colon cancer SW480 cells by decreasing the voltage-gated sodium channel subunit NaScientific reports · 2025Article
- nNav1.5 mRNA Expression in Triple Negative and Non-Triple Negative Breast Cancer Patients Treated at Hospital Pakar Universiti Sains Malaysia.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Targeting Ion Channels for Cancer Therapy: From Pathophysiological Mechanisms to Clinical Translation.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Investigation on the phenytoin sodium channel-blocker effect in PDT of MDA MB 231 breast cancer using a positively charged PS.Scientific reports · 2025Article
- Ion channel mutations and cancer.Biochemistry and biophysics reports · 2025Review
- Sodium channels in non-excitable cells: powerful actions and therapeutic targets beyond Hodgkin and Huxley.Trends in cell biology · 2025Review
- Neuronal mimicry in tumors: lessons from neuroscience to tackle cancer.Cancer metastasis reviews · 2025Review
- Stemness of Cancer: A Study of Triple-negative Breast Cancer From a Neuroscience Perspective.Stem cell reviews and reports · 2025Review
- Clinical relevance of macromolecular complexes involving integrins, potassium and sodium ion channels and the sodium/proton antiporter in human breast cancer.Cancer cell international · 2025Article
- Review of electrophysiological models to study membrane potential changes in breast cancer cell transformation and tumor progression.Frontiers in physiology · 2025Review
- Insights into the Emerging Therapeutic Targets of Triple-negative Breast Cancer.Current cancer drug targets · 2025Review
- Electrical excitability of cancer cells-CELEX model updated.Cancer metastasis reviews · 2024Review
- Potential Shortcomings of Genomic Database: The Case of NaBioelectricity · 2024Article
- A novel NaOncogene · 2024Article
- Voltage-gated sodium channels in cancers.Biomarker research · 2024Review
- The role of lidocaine in cancer progression and patient survival.Pharmacology & therapeutics · 2024Review
- Ranolazine: a potential anti-metastatic drug targeting voltage-gated sodium channels.British journal of cancer · 2024Review
32 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Upregulation of functional voltage-gated Na+ channels (VGSCs) occurs in metastatic human breast cancer (BCa) in vitro and in vivo. The present study aimed to ascertain the specific involvement of the "neonatal" splice variant of Nav1.5 (nNav1.5), thought to be predominant, in the VGSC-dependent invasive behaviour of MDA-MB-231 cells. Functional activity of nNav1.5 was suppressed by two different methods targeting nNav1.5: (i) small interfering RNA (siRNA), and (ii) a polyclonal antibody (NESO-pAb); effects upon migration and invasion were determined. nNav1.5 mRNA, protein and signalling were measured using real-time PCR, Western blotting, and patch clamp recording, respectively. Treatment with the siRNA rapidly reduced (by approximately 90%) the level of nNav1.5 (but not adult Nav1.5) mRNA, but the protein reduction was much smaller (approximately 30%), even after 13 days. Nevertheless, the siRNA reduced peak VGSC current density by 33%, and significantly increased the cells' sensitivity to nanomolar tetrodotoxin (TTX). Importantly, the siRNA suppressed in vitro migration by 43%, and eliminated the normally inhibitory effect of TTX. Migrated MDA-MB-231 cells expressed more nNav1.5 protein at the plasma membrane than non-migrated cells. Furthermore, NESO-pAb reduced migration by up to 42%, in a dose-dependent manner. NESO-pAb also reduced Matrigel invasion without affecting proliferation. TTX had no effect on cells already treated with NESO-pAb. It was concluded that nNav1.5 is primarily responsible for the VGSC-dependent enhancement of invasive behaviour in MDA-MB-231 cells. Accordingly, targeting nNav1.5 expression/activity may be useful in clinical management of metastatic BCa.
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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.