Evidence map›Paper›PMID 27065322›Full record

ArticleOncogene2016

In vivo overexpression of Emi1 promotes chromosome instability and tumorigenesis.

S Vaidyanathan, K Cato, L Tang, S Pavey, N K Haass, B G Gabrielli, P H G Duijf

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. 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
4.5field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 103 citations in OpenAlex.

  1. Mutation Severity ofHuman mutation · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Examining the mechanistic relationship of APC/CProtein science : a publication of the Protein Society · 2022
    Article
  11. Article
  12. PRUNE2 inhibits progression of colorectal cancerExperimental and therapeutic medicine · 2022
    Article
  13. Article
  14. Article
  15. The role of Fbxo5 in the development of human malignant tumors.American journal of cancer research · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

7 authors at 2 institutions in 2 countries.

S VaidyanathanUniversity of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia.
K CatoUniversity of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia.
L TangUniversity of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia.
S PaveyUniversity of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia.
N K HaassUniversity of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia.
B G GabrielliUniversity of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia.
P H G DuijfUniversity of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia.
Translational Research Institute · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell cycle genes are often aberrantly expressed in cancer, but how their misexpression drives tumorigenesis mostly remains unclear. From S phase to early mitosis, EMI1 (also known as FBXO5) inhibits the anaphase-promoting complex/cyclosome, which controls cell cycle progression through the sequential degradation of various substrates. By analyzing 7403 human tumor samples, we find that EMI1 overexpression is widespread in solid tumors but not in blood cancers. In solid cancers, EMI1 overexpression is a strong prognostic marker for poor patient outcome. To investigate causality, we generated a transgenic mouse model in which we overexpressed Emi1. Emi1-overexpressing animals develop a wide variety of solid tumors, in particular adenomas and carcinomas with inflammation and lymphocyte infiltration, but not blood cancers. These tumors are significantly larger and more penetrant, abundant, proliferative and metastatic than control tumors. In addition, they are highly aneuploid with tumor cells frequently being in early mitosis and showing mitotic abnormalities, including lagging and incorrectly segregating chromosomes. We further demonstrate in vitro that even though EMI1 overexpression may cause mitotic arrest and cell death, it also promotes chromosome instability (CIN) following delayed chromosome alignment and anaphase onset. In human solid tumors, EMI1 is co-expressed with many markers for CIN and EMI1 overexpression is a stronger marker for CIN than most well-established ones. The fact that Emi1 overexpression promotes CIN and the formation of solid cancers in vivo indicates that Emi1 overexpression actively drives solid tumorigenesis. These novel mechanistic insights have important clinical implications.

Indexed as

Anaphase-Promoting Complex-CyclosomeAnimalsBiomarkers, TumorCarcinogenesisCell Cycle ProteinsChromosomal InstabilityF-Box ProteinsGene Expression Regulation, NeoplasticHumansMiceMice, TransgenicMitosisNeoplasmsPhosphorylationAnaphase-Promoting Complex-CyclosomeBiomarkers, TumorCell Cycle ProteinsF-Box ProteinsFBXO5 protein, human

Identifiers

PMID27065322
OpenAlexW2327288796

What OpenQuestion holds

Textmetadata
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.