Evidence map›Paper›PMID 35488278›Full record

ArticleBiological research2022

nNav1.5 expression is associated with glutamate level in breast cancer cells.

Irfan Irsyad Azahar, Nur Aishah Sharudin, Ahmad Hafiz Murtadha Noor Din, Ahmad Tarmizi Che Has, Siti Norasikin Mohd Nafi, Hasnan Jaafar, Noor Fatmawati Mokhtar

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 34% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Irfan Irsyad AzaharInstitute for Research in Molecular Medicine (INFORMM), Universiti Sains Malaysia, Health Campus, 16150, Kubang Kerian, Kelantan, Malaysia.
Nur Aishah SharudinInstitute for Research in Molecular Medicine (INFORMM), Universiti Sains Malaysia, Health Campus, 16150, Kubang Kerian, Kelantan, Malaysia.
Ahmad Hafiz Murtadha Noor DinInstitute for Research in Molecular Medicine (INFORMM), Universiti Sains Malaysia, Health Campus, 16150, Kubang Kerian, Kelantan, Malaysia.
Ahmad Tarmizi Che HasDepartment of Neuroscience, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, 16150, Kubang Kerian, Kelantan, Malaysia.
Siti Norasikin Mohd NafiDepartment of Pathology, School of Medical Sciences, Universiti Sains Malaysia, Health, Kelantan, Malaysia.
Hasnan JaafarDepartment of Pathology, School of Medical Sciences, Universiti Sains Malaysia, Health, Kelantan, Malaysia.
Noor Fatmawati MokhtarInstitute for Research in Molecular Medicine (INFORMM), Universiti Sains Malaysia, Health Campus, 16150, Kubang Kerian, Kelantan, Malaysia. fatmawati@usm.my.ORCID http://orcid.org/0000-0003-0349-4096
Universiti Sains Malaysia · MY

Funding

Ministry of Education, Malaysia Research University Grant 1001/CIPPM/8012235
6 · The paper itself

Abstract

backgroundGlutamate and voltage-gated sodium channels, both have been the target of intense investigation for its involvement in carcinogenesis and progression of malignant disease. Breast cancer with increased level of glutamate often metastasize to other organs (especially bone), whilst re-expression of 'neonatal' Nav1.5, nNav1.5 in breast cancer is known to promote cell invasion in vitro, metastasis in vivo and positive lymph node metastasis in patients.

methodsIn this study, the role of nNav1.5 in regulating glutamate level in human breast cancer cells was examined using pharmacological approach (VGSCs specific blocker, TTX, glutamate release inhibitor, riluzole and siRNA-nNav1.5). Effect of these agents were evaluated based on endogenous and exogenous glutamate concentration using glutamate fluorometric assay, mRNA expression of nNav1.5 using qPCR and finally, invasion using 3D culture assay.

resultsEndogenous and exogenous glutamate levels were significantly higher in aggressive human breast cancer cells, MDA-MB-231 cells compared to less aggressive human breast cancer cells, MCF-7 and non-cancerous human breast epithelial cells, MCF-10A. Treatment with TTX to MDA-MB-231 cells resulted in significant reduction of endogenous and exogenous glutamate levels corresponded with significant suppression of cell invasion. Subsequently, downregulation of nNav1.5 gene was observed in TTX-treated cells.

conclusionsAn interesting link between nNav1.5 expression and glutamate level in aggressive breast cancer cells was detected and requires further investigation.

Indexed as

Breast NeoplasmsCell Line, TumorFemaleGlutamic AcidHumansInfant, NewbornNAV1.5 Voltage-Gated Sodium ChannelRNA, Small InterferingGlutamic AcidNAV1.5 Voltage-Gated Sodium ChannelRNA, Small InterferingBreast cancerEndogenous glutamateExogenous glutamateInvasionNeonatal Nav1.5Voltage-gated sodium channels

Identifiers

PMID35488278
PMCPMC9052458
OpenAlexW4225162022

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.