ArticleInternational journal of oncology2016
Blockade of voltage-gated sodium channels inhibits invasion of endocrine-resistant breast cancer cells.
Article in International journal of oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 47 citations in OpenAlex.
- Inflammatory Co-Regulation of Voltage-Gated Sodium Channels and Na,K-ATPase in Metastatic Breast Cancer.International journal of molecular sciences · 2025Article
- Bioactivity-guided fractionation of Withania somnifera (L.) Dunal roots extract: evaluation of the anti-progressive potential on human Kelly neuroblastoma cell line.BMC complementary medicine and therapies · 2025Article
- Effects of NaCell biochemistry and biophysics · 2025Review
- The Multiscale Wisdom of the Body: Collective Intelligence as a Tractable Interface for Next-Generation Biomedicine.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Modulating voltage-gated sodium channels to enhance differentiation and sensitize glioblastoma cells to chemotherapy.Cell communication and signaling : CCS · 2024Article
- A novel NaOncogene · 2024Article
- The role of lidocaine in cancer progression and patient survival.Pharmacology & therapeutics · 2024Review
- Hydroquinidine displays a significant anticarcinogenic activity in breast and ovarian cancer cells via inhibiting cell-cycle and stimulating apoptosis.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- From HDAC to Voltage-Gated Ion Channels: What's Next? The Long Road of Antiepileptic Drugs Repositioning in Cancer.Cancers · 2022Review
- Combinatorial Therapy of Cancer: Possible Advantages of Involving Modulators of Ionic Mechanisms.Cancers · 2022Review
- Discovering the Triad between Nav1.5, Breast Cancer, and the Immune System: A Fundamental Review and Future Perspectives.Biomolecules · 2022Review
- Phenytoin Regulates Migration and Osteogenic Differentiation by MAPK Pathway in Human Periodontal Ligament Cells.Cellular and molecular bioengineering · 2022Article
- Ion Transporting Proteins and Cancer: Progress and Perspectives.Reviews of physiology, biochemistry and pharmacology · 2022Article
- Ion Transport and Radioresistance.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Review
- Ion Channel Regulation by Sex Steroid Hormones and Vitamin D in Cancer: A Potential Opportunity for Cancer Diagnosis and Therapy.Frontiers in pharmacology · 2020Review
- The Functional Role of Voltage-Gated Sodium Channel Nav1.5 in Metastatic Breast Cancer.Frontiers in pharmacology · 2020Review
- Nav1.5-E3 antibody inhibits cancer progression.Translational cancer research · 2019Article
- The invasiveness of human cervical cancer associated to the function of NaScientific reports · 2018Article
- The influence of sodium on pathophysiology of multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Voltage-gated Na+ channels (VGSCs) are membrane proteins which are normally expressed in excitable cells but have also been detected in cancer cells, where they are thought to be involved in malignancy progression. In this study we examined the ion current and expression profile of VGSC (Nav1.5) in estrogen receptor (ER)-positive (MCF-7) and silenced (pII) breast cancer cells and its possible influence on their proliferation, motility and invasion. VGSC currents were analysed by whole cell patch clamp recording. Nav1.5 expression and localization, in response to EGF stimulation, was examined by western blotting and immunofluorescence respectively. Cell invasion (under-agarose and Matrigel assays), motility (wound healing assay) and proliferation (MTT assay) were assessed in pII cells in response to VGSC blockers, phenytoin (PHT) and tetrodotoxin (TTX), or by siRNA knockdown of Nav1.5. The effect of PHT and TTX on modulating EGF-induced phosphorylation of Akt and ERK1/2 was determined by western blotting. Total matrix metalloproteinase (MMP) was determined using a fluorometric-based activity assay. The level of various human proteases was detected by using proteome profiler array kit. VGSC currents were detected in pII cells, but were absent in MCF-7. Nav1.5 showed cytoplasmic and perinuclear expression in both MCF-7 and pII cells, with enhanced expression upon EGF stimulation. Treatment of pII cells with PHT, TTX or siRNA significantly reduced invasion towards serum components and EGF, in part through reduction of P-ERK1/2 and proteases such as cathepsin E, kallikrein-10 and MMP-7, as well as total MMP activity. At high concentrations, PHT inhibited motility while TTX reduced cell proliferation. Pharmacological or genetic blockade of Nav1.5 may serve as a potential anti-metastatic therapy for breast cancer.
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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.