Evidence map›Paper›PMID 29615116›Full record

ArticleBMC research notes2018

Expression and in vitro assessment of tumorigenicity for NOD1 and NOD2 receptors in breast cancer cell lines.

Fernando J Velloso, Mari Cleide Sogayar, Ricardo G Correa

Open access · goldAbstract read
In one paragraph

Article in BMC research notes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Evidence of a synthetic lethality interaction between SETDB1 histone methyltransferase and CHD4 chromatin remodeling protein in a triple negative breast cancer cell line.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

3 authors at 2 institutions in 2 countries.

Fernando J VellosoCell and Molecular Therapy Center (NUCEL-NETCEM), Internal Medicine Department, School of Medicine, University of São Paulo (USP), São Paulo, SP, 05360-130, Brazil.
Mari Cleide SogayarCell and Molecular Therapy Center (NUCEL-NETCEM), Internal Medicine Department, School of Medicine, University of São Paulo (USP), São Paulo, SP, 05360-130, Brazil.
Ricardo G CorreaSanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Rd., La Jolla, CA, 92037, USA. rcorrea@sbpdiscovery.org.ORCID http://orcid.org/0000-0001-6940-7034
Universidade de São Paulo · BRSanford Burnham Prebys Medical Discovery Institute · US

Funding

Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI ELENA B PASQUALE · 1985 to 2026
$107.2M
CAPES Science without BordersNCI NIH HHS P30 CA030199
6 · The paper itself

Abstract

objectiveImmune-related pathways have been frequently associated to tumorigenesis. NOD1 and NOD2 are innate immune receptors responsible for sensing a subset of bacterial-derived components, and to further translate these pathogenic signals through pro-inflammatory and survival pathways. NOD1 and NOD2 have been further associated with tumorigenesis, particularly in gastrointestinal cancers. NOD1 has also been suggested to be a tumor suppressor gene in a model of estrogen receptor-dependent breast cancer. Contrarily, NOD2 polymorphisms are associated with higher risk of breast cancer, with no tumor suppressor role being reported. To better delineate this issue, we investigated NOD1 and NOD2 expression in a panel of breast cancer cell lines, as well as their potential impact in breast tumorigenesis based on in vitro assays.

resultsThe highly invasive Hs578T breast cell line presented the second highest NOD1 expression and the lowest NOD2 expression in our panel. Therefore, we investigated whether NOD1 and/or NOD2 might act as a tumor suppressor in this cell model. Our studies indicate that overexpression of either NOD1 or NOD2 reduces cell proliferation and increases clonogenic potential in vitro. Elucidation of NOD1 and NOD2 effects on tumor cell viability and proliferation may unveil potential targets for future therapeutic intervention.

Indexed as

Gene Expression ProfilingBreast NeoplasmsCarcinogenicity TestsCell Line, TumorFemaleHumansNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinNOD1 protein, humanNod1 Signaling Adaptor ProteinNOD2 protein, humanNod2 Signaling Adaptor ProteinBreast cancerHs578TMDPNLRNOD1NOD2γ-Tri-DAP

Identifiers

PMID29615116
PMCPMC5883347
OpenAlexW2799320629

What Socratic 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 Socratic graph.