Evidence map›Paper›PMID 26996665›Full record

ArticleOncogene2016

The Δ133p53 isoform and its mouse analogue Δ122p53 promote invasion and metastasis involving pro-inflammatory molecules interleukin-6 and CCL2.

I Roth, H Campbell, C Rubio, C Vennin, M Wilson, A Wiles, G Williams, A Woolley, P Timpson, M V Berridge and 3 more

Abstract 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-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

31 citing papers in PubMed, 38 citations in OpenAlex.

  1. The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Increased Expression of the Δ133p53β Isoform Enhances Brain Metastasis.International journal of molecular sciences · 2023
    Article
  7. Review
  8. p53 Family in Resistance to Targeted Therapy of Melanoma.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Conformational stability and dynamics of the cancer-associated isoform Δ133p53β are modulated by p53 peptides and p53-specific DNA.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  20. A mouse model of the Δ133p53 isoform: roles in cancer progression and inflammation.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
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

13 authors at 6 institutions in 2 countries.

I RothDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
H CampbellChildren's Medical Research Institute, University of Sydney, Sydney, New South Wales, Australia.
C RubioChildren's Medical Research Institute, University of Sydney, Sydney, New South Wales, Australia.
C VenninThe Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
M WilsonDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
A WilesDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
G WilliamsDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
A WoolleyDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
P TimpsonThe Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
M V BerridgeMalaghan Institute for Medical Research, Wellington, New Zealand.
N FlemingDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
M BairdDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
A W BraithwaiteDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
University of Otago · NZGarvan Institute of Medical Research · AUMaurice Wilkins Centre · NZChildren's Medical Research Institute · AUMalaghan Institute of Medical Research · NZUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A number of naturally occurring isoforms of the tumour suppressor protein p53 have been discovered, which appear to have differing roles in tumour prevention or promotion. We are investigating the tumour-promoting activities of the Δ133p53 isoform using our mouse model of Δ133p53 (Δ122p53). Here, we report that tumours from Δ122p53 homozygous mice show evidence of invasion and metastasis and that Δ122p53 promotes migration though a 3-dimensional collagen matrix. We also show that Δ122p53 and Δ133p53 promote cell migration in scratch wound and Transwell assays, similar to the 'gain-of-function' phenotypes seen with mutant p53. Using the well-defined B16 mouse melanoma metastatic model, we show that Δ122p53 leads to faster generation of lung metastases. The increased migratory phenotypes are dependent on secreted factors, including the cytokine interleukin-6 and the chemokine CCL2. We propose that Δ122p53 (and Δ133p53) acts in a similar manner to 'gain-of-function' mutant p53 proteins to promote migration, invasion and metastasis, which may contribute to poor survival in patients with Δ133p53-expressing tumours.

Indexed as

AnimalsCell MovementChemokine CCL2HumansInterleukin-6Lung NeoplasmsMelanoma, ExperimentalMiceMutationNeoplasm InvasivenessNeoplasm MetastasisProtein IsoformsTumor Suppressor Protein p53CCL2 protein, humanChemokine CCL2Interleukin-6Protein IsoformsTumor Suppressor Protein p53

Identifiers

PMID26996665
OpenAlexW2311369088

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.