Evidence map›Paper›PMID 27427552›Full record

ReviewAsian journal of andrology

Phenotypic plasticity in prostate cancer: role of intrinsically disordered proteins.

Steven M Mooney, Mohit Kumar Jolly, Herbert Levine, Prakash Kulkarni

Abstract readReview
In one paragraph

Review in Asian journal of andrology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. The Proteomic Analysis of Cancer-Related Alterations in the Human Unfoldome.International journal of molecular sciences · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Journal of biosciences · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. The somatic molecular evolution of cancer: Mutation, selection, and epistasis.Progress in biophysics and molecular biology · 2021
    Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors.

Steven M MooneyDepartment of Biology, University of Waterloo, Waterloo, ON N2L 3G1, Canada.
Mohit Kumar JollyCenter for Theoretical Biological Physics, Rice University, Houston, TX 77005; Department of Bioengineering, Rice University, Houston, TX 77005, USA.
Herbert LevineCenter for Theoretical Biological Physics, Rice University, Houston, TX 77005; Department of Bioengineering, Rice University, Houston, TX 77005; Department of Physics and Astronomy, Rice University, Houston, TX 77005, USA.
Prakash KulkarniInstitute for Bioscience and Biotechnology Research, University of Maryland, Rockville, Maryland 20850, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A striking characteristic of cancer cells is their remarkable phenotypic plasticity, which is the ability to switch states or phenotypes in response to environmental fluctuations. Phenotypic changes such as a partial or complete epithelial to mesenchymal transition (EMT) that play important roles in their survival and proliferation, and development of resistance to therapeutic treatments, are widely believed to arise due to somatic mutations in the genome. However, there is a growing concern that such a deterministic view is not entirely consistent with multiple lines of evidence, which indicate that stochasticity may also play an important role in driving phenotypic plasticity. Here, we discuss how stochasticity in protein interaction networks (PINs) may play a key role in determining phenotypic plasticity in prostate cancer (PCa). Specifically, we point out that the key players driving transitions among different phenotypes (epithelial, mesenchymal, and hybrid epithelial/mesenchymal), including ZEB1, SNAI1, OVOL1, and OVOL2, are intrinsically disordered proteins (IDPs) and discuss how plasticity at the molecular level may contribute to stochasticity in phenotypic switching by rewiring PINs. We conclude by suggesting that targeting IDPs implicated in EMT in PCa may be a new strategy to gain additional insights and develop novel treatments for this disease, which is the most common form of cancer in adult men.

Indexed as

Epithelial-Mesenchymal TransitionHumansIntrinsically Disordered ProteinsMalePhenotypeProstatic NeoplasmsIntrinsically Disordered Proteins

Identifiers

PMID27427552
PMCPMC5000791

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.