Evidence map›Paper›PMID 24858043›Full record

ArticleOncogene2014

MCT-1 expression and PTEN deficiency synergistically promote neoplastic multinucleation through the Src/p190B signaling activation.

M-H Wu, Y-A Chen, H-H Chen, K-W Chang, I-S Chang, L-H Wang, H-L Hsu

Open access · hybridAbstract read
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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022
    Review
  5. Frontiers in genetics · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. p190RhoGAPs, theCells · 2019
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. 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.

M-H WuInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Taiwan, ROC.
Y-A ChenInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Taiwan, ROC.
H-H ChenInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Taiwan, ROC.
K-W ChangInstitute of Population Health Science, National Health Research Institutes, Taiwan, ROC.
I-S ChangNational Institute of Cancer Research and Division of Biostatistics and Bioinformatics, National Health Research Institutes, Taiwan, ROC.
L-H WangInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Taiwan, ROC.
H-L HsuInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Taiwan, ROC.
National Health Research Institutes · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multinucleation is associated with malignant neoplasms; however, the molecular mechanism underlying the nuclear abnormality remains unclear. Loss or mutation of PTEN promotes the development of malignant tumors. We now demonstrate that increased expression of the oncogene MCT-1 (multiple copies in T-cell malignancy 1) antagonizes PTEN gene presentation, PTEN protein stability and PTEN functional activity, thereby further promoting phosphoinositide 3 kinase/AKT signaling, survival rate and malignancies of the PTEN-deficient cells. In the PTEN-null cancer cells, MCT-1 interacts with p190B and Src in vivo, supporting that they are in proximity of the signaling complexes. MCT-1 overexpression and PTEN loss synergistically augments the Src/p190B signaling function that leads to inhibition of RhoA activity. Under such a condition, the incidence of mitotic catastrophes including spindle multipolarity and cytokinesis failure is enhanced, driving an Src/p190B/RhoA-dependent neoplastic multinucleation. Targeting MCT-1 by the short hairpin RNA markedly represses the Src/p190B function, improves nuclear structures and suppresses xenograft tumorigenicity of the PTEN-null breast cancer cells. Consistent with the oncogenic effects in vitro, clinical evidence has confirmed that MCT-1 gene stimulation is correlated with p190B gene promotion and PTEN gene suppression in human breast cancer. Accordingly, MCT-1 gene induction is recognized as a potential biomarker of breast tumor development. Abrogating MCT-1 function may be a promising stratagem for management of breast cancer involving Src hyperactivation and/or PTEN dysfunction.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell NucleusFemaleGene Expression Regulation, NeoplasticGTPase-Activating ProteinsHumansMCF-7 CellsMiceOncogene ProteinsProto-Oncogene Proteins pp60(c-src)PTEN PhosphohydrolaserhoA GTP-Binding ProteinSignal TransductionGTPase-Activating ProteinsOncogene ProteinsProto-Oncogene Proteins pp60(c-src)PTEN PhosphohydrolaserhoA GTP-Binding Protein

Identifiers

PMID24858043
PMCPMC4287651
OpenAlexW2009984937

What OpenQuestion holds

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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.