Evidence map›Paper›PMID 37929635›Full record

ArticleThe Journal of pathology2024

Opposing roles for ADAMTS2 and ADAMTS14 in myofibroblast differentiation and function.

Edward P Carter, Kubra K Yoneten, Nuria Gavara, Eleanor J Tyler, Valentine Gauthier, Elizabeth R Murray, Peter Ten Dijke, Angus J Cameron, Oliver Pearce, Richard P Grose

Abstract read
In one paragraph

Article in The Journal of pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. ADAMTS14 is a novel modulator of fibroblast mechanoactivation in pulmonary fibrosis.American journal of respiratory and critical care medicine · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. 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

10 authors.

Edward P CarterCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0003-4499-1101
Kubra K YonetenCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Nuria GavaraUnitat de Biofísica i Bioenginyeria, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona, Barcelona, Spain.ORCID 0000-0002-7666-110X
Eleanor J TylerCentre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0001-8945-4823
Valentine GauthierCentre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0001-7360-4305
Elizabeth R MurrayCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Peter Ten DijkeOncode Institute and Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0002-7234-342X
Angus J CameronCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0003-3906-2789
Oliver PearceCentre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0003-3953-1629
Richard P GroseCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0002-4738-0173

Funding

Cancer Research UK 27781Cancer Research UK 27947Cancer Research UK A25137Cancer Research UK A27781
6 · The paper itself

Abstract

Crosstalk between cancer and stellate cells is pivotal in pancreatic cancer, resulting in differentiation of stellate cells into myofibroblasts that drives tumour progression. To assess cooperative mechanisms in a 3D context, we generated chimeric spheroids using human and mouse cancer and stellate cells. Species-specific deconvolution of bulk-RNA sequencing data revealed cell type-specific transcriptomes underpinning invasion. This dataset highlighted stellate-specific expression of transcripts encoding the collagen-processing enzymes ADAMTS2 and ADAMTS14. Strikingly, loss of ADAMTS2 reduced, while loss of ADAMTS14 promoted, myofibroblast differentiation and invasion independently of their primary role in collagen-processing. Functional and proteomic analysis demonstrated that these two enzymes regulate myofibroblast differentiation through opposing roles in the regulation of transforming growth factor β availability, acting on the protease-specific substrates, Serpin E2 and fibulin 2, for ADAMTS2 and ADAMTS14, respectively. Showcasing a broader complexity for these enzymes, we uncovered a novel regulatory axis governing malignant behaviour of the pancreatic cancer stroma. © 2023 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

Indexed as

MyofibroblastsPancreatic NeoplasmsADAMTS ProteinsAnimalsCell DifferentiationCollagenHumansMiceProteomicsADAMTS14 protein, humanAdamts14 protein, mouseADAMTS2 protein, humanAdamts2 protein, mouseADAMTS ProteinsCollagen3D in vitro modelscancer-associated fibroblastscancer invasioncellular cross talkextracellular matrixmyofibroblastpancreatic cancerproteaseTGFβ

Identifiers

PMID37929635
PMCPMC10953099

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.