Evidence map›Paper›PMID 36892272›Full record

ArticleeLife2023

Interplay of adherens junctions and matrix proteolysis determines the invasive pattern and growth of squamous cell carcinoma.

Takuya Kato, Robert P Jenkins, Stefanie Derzsi, Melda Tozluoglu, Antonio Rullan, Steven Hooper, Raphaël A G Chaleil, Holly Joyce, Xiao Fu, Selvam Thavaraj and 2 more

Abstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Amoeboid-mesenchymal transition and the proteolytic control of cancer invasion plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Collective migration modes in development, tissue repair and cancer.Nature reviews. Molecular cell biology · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. 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

12 authors.

Takuya Kato *Tumour Cell Biology Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0002-4972-657X
Robert P Jenkins *Tumour Cell Biology Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0002-6186-7746
Stefanie DerzsiTumour Cell Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Melda TozluogluBiomolecular Modelling Laboratory, The Francis Crick Institute, London, United Kingdom.
Antonio RullanTumour Cell Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Steven HooperTumour Cell Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Raphaël A G ChaleilBiomolecular Modelling Laboratory, The Francis Crick Institute, London, United Kingdom.
Holly JoyceTumour Cell Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Xiao FuTumour Cell Biology Laboratory, The Francis Crick Institute, London, United Kingdom.
Selvam ThavarajCentre for Oral, Clinical and Translational Sciences, King's College London, London, United Kingdom.ORCID 0000-0001-5720-7422
Paul A BatesBiomolecular Modelling Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0003-0621-0925
Erik SahaiTumour Cell Biology Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0002-3932-5086

Funding

Cancer Research UK 28990Cancer Research UK FC001003Cancer Research UK FC001144Medical Research Council FC001003Medical Research Council FC001144Wellcome Trust FC001003Wellcome Trust FC001144
6 · The paper itself

Abstract

Cancers, such as squamous cell carcinoma, frequently invade as multicellular units. However, these invading units can be organised in a variety of ways, ranging from thin discontinuous strands to thick 'pushing' collectives. Here we employ an integrated experimental and computational approach to identify the factors that determine the mode of collective cancer cell invasion. We find that matrix proteolysis is linked to the formation of wide strands but has little effect on the maximum extent of invasion. Cell-cell junctions also favour wide strands, but our analysis also reveals a requirement for cell-cell junctions for efficient invasion in response to uniform directional cues. Unexpectedly, the ability to generate wide invasive strands is coupled to the ability to grow effectively when surrounded by extracellular matrix in three-dimensional assays. Combinatorial perturbation of both matrix proteolysis and cell-cell adhesion demonstrates that the most aggressive cancer behaviour, both in terms of invasion and growth, is achieved at high levels of cell-cell adhesion and high levels of proteolysis. Contrary to expectation, cells with canonical mesenchymal traits - no cell-cell junctions and high proteolysis - exhibit reduced growth and lymph node metastasis. Thus, we conclude that the ability of squamous cell carcinoma cells to invade effectively is also linked to their ability to generate space for proliferation in confined contexts. These data provide an explanation for the apparent advantage of retaining cell-cell junctions in squamous cell carcinomas.

Indexed as

Adherens JunctionsCarcinoma, Squamous CellCell Line, TumorHumansNeoplasm InvasivenessProteolysiscancer biologycellular mechanismscomputational biologycomputational modellinghumaninvasive patternmousesystems biologytumour microenvironment

Identifiers

PMID36892272
PMCPMC9998089

What Socratic 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 Socratic graph.