Evidence map›Paper›PMID 30498210›Full record

ArticleNature communications2018

Mutant p53s generate pro-invasive niches by influencing exosome podocalyxin levels.

David Novo, Nikki Heath, Louise Mitchell, Giuseppina Caligiuri, Amanda MacFarlane, Dide Reijmer, Laura Charlton, John Knight, Monika Calka, Ewan McGhee and 16 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

89 citing papers in PubMed, 132 citations in OpenAlex.

  1. Review
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  10. The fibroinflammatory response in cancer.Nature reviews. Cancer · 2025
    Review
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  19. Review
  20. Targeting the secretory program of 3q-amplified lung cancers.The Journal of clinical investigation · 2024
    Article

29 more citing papers are in PubMed but not listed here.

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

26 authors at 5 institutions in 3 countries.

David NovoBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.ORCID http://orcid.org/0000-0001-5344-0083
Nikki HeathBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Louise MitchellBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Giuseppina CaligiuriInstitute of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, UK.
Amanda MacFarlaneBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Dide ReijmerBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Laura CharltonSchool of Engineering, University of Glasgow, Glasgow, G12 8LT, UK.
John KnightBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Monika CalkaInstitute of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, UK.
Ewan McGheeBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Emmanuel DornierBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.ORCID http://orcid.org/0000-0002-3482-8637
David SumptonBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.ORCID http://orcid.org/0000-0002-9004-4079
Susan MasonBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Arnaud EchardMembrane Traffic and Cell Division Lab, Cell Biology and Infection Department, Institut Pasteur, 25-28 rue du Dr Roux, Paris, 75724, France.ORCID http://orcid.org/0000-0001-7402-1398
Kerstin KlinkertMembrane Traffic and Cell Division Lab, Cell Biology and Infection Department, Institut Pasteur, 25-28 rue du Dr Roux, Paris, 75724, France.
Judith SecklehnerBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Flore KruiswijkBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Karen VousdenBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Iain R MacphersonBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.ORCID http://orcid.org/0000-0003-4295-8885
Karen BlythBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.ORCID http://orcid.org/0000-0002-9304-439X
Peter BaileyWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, G611QH, UK.
Huabing YinSchool of Engineering, University of Glasgow, Glasgow, G12 8LT, UK.ORCID http://orcid.org/0000-0001-7693-377X
Leo M CarlinBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.ORCID http://orcid.org/0000-0001-7172-5234
Jennifer MortonBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.
Sara ZanivanBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK.ORCID http://orcid.org/0000-0002-9880-9099
Jim C NormanBeatson Institute for Cancer Research, Glasgow, G61 1BD, Scotland, UK. j.norman@beatson.gla.ac.uk.
Cancer Research UK Scotland Institute · GBUniversity of Glasgow · GBInstitut Pasteur · FRLung Institute · USThe Francis Crick Institute · GB

Funding

Cancer Research UK 12935Cancer Research UK 18277Cancer Research UK 23983Cancer Research UK 29800Medical Research Council MR/P01058X/1
6 · The paper itself

Abstract

Mutant p53s (mutp53) increase cancer invasiveness by upregulating Rab-coupling protein (RCP) and diacylglycerol kinase-α (DGKα)-dependent endosomal recycling. Here we report that mutp53-expressing tumour cells produce exosomes that mediate intercellular transfer of mutp53's invasive/migratory gain-of-function by increasing RCP-dependent integrin recycling in other tumour cells. This process depends on mutp53's ability to control production of the sialomucin, podocalyxin, and activity of the Rab35 GTPase which interacts with podocalyxin to influence its sorting to exosomes. Exosomes from mutp53-expressing tumour cells also influence integrin trafficking in normal fibroblasts to promote deposition of a highly pro-invasive extracellular matrix (ECM), and quantitative second harmonic generation microscopy indicates that this ECM displays a characteristic orthogonal morphology. The lung ECM of mice possessing mutp53-driven pancreatic adenocarcinomas also displays increased orthogonal characteristics which precedes metastasis, indicating that mutp53 can influence the microenvironment in distant organs in a way that can support invasive growth.

Indexed as

AnimalsCell LineExosomesFemaleHumansMiceMice, NudeMicroscopy, Atomic ForceMutationrab GTP-Binding ProteinsSialoglycoproteinsSialomucinsTumor Suppressor Protein p53podocalyxinrab GTP-Binding ProteinsSialoglycoproteinsSialomucinsTumor Suppressor Protein p53

Identifiers

PMID30498210
PMCPMC6265295
OpenAlexW2901794628

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.