Evidence map›Paper›PMID 23770854›Full record

ArticleOncogene2014

Loss of N-Myc interactor promotes epithelial-mesenchymal transition by activation of TGF-β/SMAD signaling.

D J Devine, J W Rostas, B J Metge, S Das, M S Mulekar, J A Tucker, W E Grizzle, D J Buchsbaum, L A Shevde, R S Samant

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Genetic variants in N-myc (and STAT) interactor and susceptibility to glioma in a Chinese Han population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  17. Article
  18. NMI and EMT.Oncoscience · 2014
    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

10 authors.

D J DevineMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
J W Rostas1] Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA [2] Department of Surgery, University of South Alabama, Mobile, AL, USA.
B J MetgeDepartment of Pathology and Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
S DasDepartment of Pathology and Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
M S MulekarDepartment of Mathematics and Statistics, University of South Alabama, Mobile, AL, USA.
J A TuckerDepartment of Pathology, University of South Alabama, Mobile, AL, USA.
W E GrizzleDepartment of Pathology and Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
D J BuchsbaumDepartment of Radiation Oncology, University of Alabama at Birmingham, AL, USA.
L A ShevdeDepartment of Pathology and Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
R S SamantDepartment of Pathology and Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.

Funding

Molecular determinants of breast cancer malignancyR01CA138850 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SHEVDE, LALITA A. · 2011 to 2015
$1.6M
Role of Nmi in retarding breast tumor growth.R01CA140472 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SAMANT, RAJEEV S · 2010 to 2014
$1.3M
NCI NIH HHS CA138850NCI NIH HHS CA140472NCI NIH HHS R01 CA138850NCI NIH HHS R01 CA140472
6 · The paper itself

Abstract

Epithelial-mesenchymal transition is one of the critical cellular programs that facilitate the progression of breast cancer to an invasive disease. We have observed that the expression of N-myc interactor (NMI) decreases significantly during progression of breast cancer, specifically in invasive and metastatic stages. Recapitulation of this loss in breast cell lines with epithelial morphology (MCF10A (non-tumorigenic) and T47D (tumorigenic)) by silencing NMI expression causes mesenchymal-like morphological changes in 3D growth, accompanied by upregulation of SLUG and ZEB2 and increased invasive properties. Conversely, we found that restoring NMI expression attenuated the mesenchymal attributes of metastatic breast cancer cells, accompanied by distinctly circumscribed 3D growth with basement membrane deposition and decreased invasion. Further investigations into the downstream signaling modulated by NMI revealed that NMI expression negatively regulates SMAD signaling, which is a key regulator of cellular plasticity. We demonstrate that NMI blocks TGF-β/SMAD signaling via upregulation of SMAD7, a negative feedback regulator of the pathway. We also provide evidence that NMI activates STAT signaling, which negatively modulates TGF-β/SMAD signaling. Taken together, our findings suggest that loss of NMI during breast cancer progression could be one of the driving factors that enhance the invasive ability of breast cancer by aberrant activation of TGF-β/SMAD signaling.

Indexed as

Epithelial-Mesenchymal TransitionSignal TransductionCell LineGene SilencingHumansProto-Oncogene Proteins c-mycSmad ProteinsTransforming Growth Factor betaUp-RegulationProto-Oncogene Proteins c-mycSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID23770854
PMCPMC4267223

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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.