Evidence map›Paper›PMID 27655693›Full record

ArticleOncotarget2016

Somatic polyploidy is associated with the upregulation of c-MYC interacting genes and EMT-like signature.

Alejandro Vazquez-Martin, Olga V Anatskaya, Alessandro Giuliani, Jekaterina Erenpreisa, Sui Huang, Kristine Salmina, Inna Inashkina, Anda Huna, Nikolai N Nikolsky, Alexander E Vinogradov

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  4. Article
  5. Polyploidy and Senescence of Cancer Cells: Impact of Cell Fusion.Advances in experimental medicine and biology · 2026
    Review
  6. Article
  7. Tetraploidization Increases the Motility and Invasiveness of Cancer Cells.International journal of molecular sciences · 2023
    Article
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  9. Article
  10. Article
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  19. Article
  20. Cancer recurrence and lethality are enabled by enhanced survival and reversible cell cycle arrest of polyaneuploid cells.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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 at 4 institutions in 4 countries.

Alejandro Vazquez-MartinLatvian Biomedical Research and Study Centre, Riga, Latvia.
Olga V AnatskayaInstitute of Cytology, St-Petersburg, Russian Federation, Russia.
Alessandro GiulianiIstituto Superiore di Sanità, Rome, Italy.
Jekaterina ErenpreisaLatvian Biomedical Research and Study Centre, Riga, Latvia.
Sui HuangSystems Biology Institute, Seattle, USA.
Kristine SalminaLatvian Biomedical Research and Study Centre, Riga, Latvia.
Inna InashkinaLatvian Biomedical Research and Study Centre, Riga, Latvia.
Anda HunaLatvian Biomedical Research and Study Centre, Riga, Latvia.
Nikolai N NikolskyInstitute of Cytology, St-Petersburg, Russian Federation, Russia.
Alexander E VinogradovInstitute of Cytology, St-Petersburg, Russian Federation, Russia.
Latvian Biomedical Research and Study Centre · LVInstitute of Cytology · RUIstituto Superiore di Sanità · ITSeattle University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dependence of cancer on overexpressed c-MYC and its predisposition for polyploidy represents a double puzzle. We address this conundrum by cross-species transcription analysis of c-MYC interacting genes in polyploid vs. diploid tissues and cells, including human vs. mouse heart, mouse vs. human liver and purified 4n vs. 2n mouse decidua cells. Gene-by-gene transcriptome comparison and principal component analysis indicated that c-MYC interactants are significantly overrepresented among ploidy-associated genes. Protein interaction networks and gene module analysis revealed that the most upregulated genes relate to growth, stress response, proliferation, stemness and unicellularity, as well as to the pathways of cancer supported by MAPK and RAS coordinated pathways. A surprising feature was the up-regulation of epithelial-mesenchymal transition (EMT) modules embodied by the N-cadherin pathway and EMT regulators from SNAIL and TWIST families. Metabolic pathway analysis also revealed the EMT-linked features, such as global proteome remodeling, oxidative stress, DNA repair and Warburg-like energy metabolism. Genes associated with apoptosis, immunity, energy demand and tumour suppression were mostly down-regulated. Noteworthy, despite the association between polyploidy and ample features of cancer, polyploidy does not trigger it. Possibly it occurs because normal polyploidy does not go that far in embryonalisation and linked genome destabilisation. In general, the analysis of polyploid transcriptome explained the evolutionary relation of c-MYC and polyploidy to cancer.

Indexed as

Epistasis, GeneticGene Expression RegulationPolyploidyAnimalsCarrier ProteinsEpithelial-Mesenchymal TransitionFemaleGene DosageHepatocytesHumansLiverMetabolomicsMiceModels, BiologicalMyocardiumNuclear ProteinsCarrier ProteinsNuclear ProteinsProto-Oncogene Proteins c-mycTransforming Growth Factor betac-MYC interacting genesEMTpolyploidystressWarburg

Identifiers

PMID27655693
PMCPMC5342737
OpenAlexW2522634393

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.