Evidence map›Paper›PMID 36546396›Full record

ArticleJournal of cell science2022

Collagen VI expression is negatively mechanosensitive in pancreatic cancer cells and supports the metastatic niche.

Vasileios Papalazarou, James Drew, Amelie Juin, Heather J Spence, Jamie Whitelaw, Colin Nixon, Manuel Salmeron-Sanchez, Laura M Machesky

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. The Multifaced Role of Collagen in Cancer Development and Progression.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

8 authors at 2 institutions in 1 country.

Vasileios PapalazarouCancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK.ORCID 0000-0003-3206-401X
James DrewCancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK.ORCID 0000-0002-2864-7987
Amelie JuinCancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK.ORCID 0000-0002-1481-000X
Heather J SpenceCancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK.
Jamie WhitelawCancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK.ORCID 0000-0001-6739-1032
Colin NixonCancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK.
Manuel Salmeron-SanchezCentre for the Cellular Microenvironment, University of Glasgow,Glasgow G11 6EW, UK.ORCID 0000-0002-8112-2100
Laura M MacheskyCancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK.ORCID 0000-0002-7592-9856
Cancer Research UK · GBUniversity of Glasgow · GB

Funding

Cancer Research UK 24452Cancer Research UK A18076Cancer Research UK A24452
6 · The paper itself

Abstract

Pancreatic cancer is a deadly and highly metastatic disease, although how metastatic lesions establish is not fully understood. A key feature of pancreatic tumours is extensive fibrosis and deposition of extracellular matrix (ECM). While pancreatic cancer cells are programmed by stimuli derived from a stiff ECM, metastasis requires loss of attachment and adaptation to a softer microenvironment at distant sites. Growing evidence suggests that stiff ECM influences pancreatic cancer cell behaviour. Here, we argue that this influence is reversible and that pancreatic cancer cells can be reprogrammed upon sensing soft substrates. Using engineered polyacrylamide hydrogels with tuneable mechanical properties, we show that collagen VI is specifically upregulated in pancreatic cancer cells on soft substrates, due to a lack of integrin engagement. Furthermore, the expression of collagen VI is inversely correlated with mechanosensing and activity of YAP (also known as YAP1), which might be due to a direct or indirect effect on transcription of genes encoding collagen VI. Collagen VI supports migration in vitro and metastasis formation in vivo. Metastatic nodules formed by pancreatic cancer cells lacking Col6a1 display stromal cell-derived collagen VI deposition, suggesting that collagen VI derived from either cancer cells or the stroma is an essential component of the metastatic niche. This article has an associated First Person interview with Vasileios Papalazarou, joint first author of the paper.

Indexed as

CollagenPancreatic NeoplasmsExtracellular MatrixHumansIntegrinsTumor MicroenvironmentCollagenIntegrinsCancer metastasisCollagen VIExtracellular matrixIntegrin adhesionMechanosensingPancreatic cancer

Identifiers

PMID36546396
PMCPMC9845737
OpenAlexW4312190525

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.