ArticleOncotarget2015
Nav1.5 regulates breast tumor growth and metastatic dissemination in vivo.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 114 citations in OpenAlex.
- Sodium accumulation in breast cancer predicts malignancy and treatment response.British journal of cancer · 2022Trial
- Late IMedicinal research reviews · 2026Review
- Cancer Neuroscience: From Local Neuro-Immune Microenvironments to Systemic Brain-Body Circuitry.MedComm · 2026Review
- 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
- Effects of NaCell biochemistry and biophysics · 2025Review
- Design, Synthesis, and Evaluation of Sodium Channel Blockers with Anti-invasive Activities in Medullary Thyroid Cancer.ACS medicinal chemistry letters · 2025Article
- Neuronal mimicry in tumors: lessons from neuroscience to tackle cancer.Cancer metastasis reviews · 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
- Electrical excitability of cancer cells-CELEX model updated.Cancer metastasis reviews · 2024Review
- Role of SIK1 in tumors: Emerging players and therapeutic potentials (Review).Oncology reports · 2024Review
- A novel NaOncogene · 2024Article
- Voltage-gated sodium channels in cancers.Biomarker research · 2024Review
- Advances in the role of ion channels in leukemia.Heliyon · 2024Review
- Nanotechnology and Cancer Bioelectricity: Bridging the Gap Between Biology and Translational Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Roles of salt‑inducible kinases in cancer (Review).International journal of oncology · 2023Review
- Review
- Sodium channels and the ionic microenvironment of breast tumours.The Journal of physiology · 2023Article
- Sodium regulates PLC and IPPhysiological reports · 2023Article
- From HDAC to Voltage-Gated Ion Channels: What's Next? The Long Road of Antiepileptic Drugs Repositioning in Cancer.Cancers · 2022Review
- Invasion and Metastasis Suppression by Anti-Neonatal Nav1.5 Antibodies in Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2022Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Voltage-gated Na+ channels (VGSCs) mediate action potential firing and regulate adhesion and migration in excitable cells. VGSCs are also expressed in cancer cells. In metastatic breast cancer (BCa) cells, the Nav1.5 α subunit potentiates migration and invasion. In addition, the VGSC-inhibiting antiepileptic drug phenytoin inhibits tumor growth and metastasis. However, the functional activity of Nav1.5 and its specific contribution to tumor progression in vivo has not been delineated. Here, we found that Nav1.5 is up-regulated at the protein level in BCa compared with matched normal breast tissue. Na+ current, reversibly blocked by tetrodotoxin, was retained in cancer cells in tumor tissue slices, thus directly confirming functional VGSC activity in vivo. Stable down-regulation of Nav1.5 expression significantly reduced tumor growth, local invasion into surrounding tissue, and metastasis to liver, lungs and spleen in an orthotopic BCa model. Nav1.5 down-regulation had no effect on cell proliferation or angiogenesis within the in tumors, but increased apoptosis. In vitro, Nav1.5 down-regulation altered cell morphology and reduced CD44 expression, suggesting that VGSC activity may regulate cellular invasion via the CD44-src-cortactin signaling axis. We conclude that Nav1.5 is functionally active in cancer cells in breast tumors, enhancing growth and metastatic dissemination. These findings support the notion that compounds targeting Nav1.5 may be useful for reducing metastasis.
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.