Evidence map›Paper›PMID 23097628›Full record

ArticleNeoplasia (New York, N.Y.)2012

Bone marrow-derived myofibroblasts are the providers of pro-invasive matrix metalloproteinase 13 in primary tumor.

Julie Lecomte, Anne Masset, Silvia Blacher, Ludovic Maertens, André Gothot, Marie Delgaudine, Françoise Bruyère, Oriane Carnet, Jenny Paupert, Martin Illemann and 4 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Mechanobiological Implications of Cancer Progression in Space.Frontiers in cell and developmental biology · 2021
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Tissue Inhibitor of Metalloproteinase-1 Is Confined to Tumor-Associated Myofibroblasts and Is Increased With Progression in Gastric Adenocarcinoma.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016
    Article
  12. Review
  13. Review
  14. Bone metastasis and the metastatic niche.Journal of molecular medicine (Berlin, Germany) · 2015
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

14 authors at 4 institutions in 3 countries.

Julie LecomteLaboratory of Tumor and Development Biology, GIGA-Cancer, University of Liège, Liège, Belgium.
Anne Masset
Silvia Blacher
Ludovic Maertens
André Gothot
Marie Delgaudine
Françoise Bruyère
Oriane Carnet
Jenny Paupert
Martin Illemann
Jean-Michel Foidart
Ida K Lund
Gunilla Høyer-Hansen
Agnes Noel
University of Liège · BECopenhagen University Hospital · DKUniversity of Copenhagen · DKVlaams Instituut voor Biotechnologie · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carcinoma-associated fibroblasts are key contributors of the tumor microenvironment that regulates carcinoma progression. They consist of a heterogeneous cell population with diverse origins, phenotypes, and functions. In the present report, we have explored the contribution of bone marrow (BM)-derived cells to generate different fibroblast subsets that putatively produce the matrix metalloproteinase 13 (MMP13) and affect cancer cell invasion. A murine model of skin carcinoma was applied to mice, irradiated, and engrafted with BM isolated from green fluorescent protein (GFP) transgenic mice. We provide evidence that one third of BM-derived GFP(+) cells infiltrating the tumor expressed the chondroitin sulfate proteoglycan NG2 (pericytic marker) or α-smooth muscle actin (α-SMA, myofibroblast marker), whereas almost 90% of Thy1(+) fibroblasts were originating from resident GFP-negative cells. MMP13producing cells were exclusively α-SMA(+) cells and derived from GFP(+) BM cells. To investigate their impact on tumor invasion, we isolated mesenchymal stem cells (MSCs) from the BM of wild-type and MMP13-deficient mice. Wild-type MSC promoted cancer cell invasion in a spheroid assay, whereas MSCs obtained from MMP13-deficient mice failed to. Our data support the concept of fibroblast subset specialization with BM-derived α-SMA(+) cells being the main source of MMP13, a stromal mediator of cancer cell invasion.

Indexed as

AnimalsBiomarkers, TumorBlotting, WesternBone MarrowFemaleFibroblastsFlow CytometryHumansImmunoenzyme TechniquesIn Situ HybridizationMatrix Metalloproteinase 13Mesenchymal Stem CellsMiceMice, Inbred C57BLMice, TransgenicMyofibroblastsBiomarkers, TumorMatrix Metalloproteinase 13Mmp13 protein, mouseRNA, Messenger

Identifiers

PMID23097628
PMCPMC3479839
OpenAlexW1247179222

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.