Evidence map›Paper›PMID 20813052›Full record

ArticleMolecular cancer2010

Sprouty1, a new target of the angiostatic agent 16K prolactin, negatively regulates angiogenesis.

Céline Sabatel, Anne M Cornet, Sébastien P Tabruyn, Ludovic Malvaux, Karolien Castermans, Joseph A Martial, Ingrid Struman

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Synergistic Antitumor Effect ofMolecules (Basel, Switzerland) · 2023
    Article
  4. The Role of MicroRNA in the Pathogenesis of Diabetic Nephropathy.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. The developing story of Sprouty and cancer.Cancer metastasis reviews · 2014
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Cardiac myocyte-fibroblast interactions and the coronary vasculature.Journal of cardiovascular translational research · 2012
    Review
  15. Article
  16. 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

7 authors at 1 institution in 1 country.

Céline SabatelUnit of Molecular Biology and Genetic Engineering, GIGA-research, University of Liège, B34, Avenue de l'Hôpital, 1, Liège, Belgium.
Anne M Cornet
Sébastien P Tabruyn
Ludovic Malvaux
Karolien Castermans
Joseph A Martial
Ingrid Struman
University of Liège · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDisorganized angiogenesis is associated with several pathologies, including cancer. The identification of new genes that control tumor neovascularization can provide novel insights for future anti-cancer therapies. Sprouty1 (SPRY1), an inhibitor of the MAPK pathway, might be one of these new genes. We identified SPRY1 by comparing the transcriptomes of untreated endothelial cells with those of endothelial cells treated by the angiostatic agent 16 K prolactin (16 K hPRL). In the present study, we aimed to explore the potential function of SPRY1 in angiogenesis.

resultsWe confirmed 16 K hPRL induced up-regulation of SPRY1 in primary endothelial cells. In addition, we demonstrated the positive SPRY1 regulation in a chimeric mouse model of human colon carcinoma in which 16 K hPRL treatment was shown to delay tumor growth. Expression profiling by qRT-PCR with species-specific primers revealed that induction of SPRY1 expression by 16 K hPRL occurs only in the (murine) endothelial compartment and not in the (human) tumor compartment. The regulation of SPRY1 expression was NF-κB dependent. Partial SPRY1 knockdown by RNA interference protected endothelial cells from apoptosis as well as increased endothelial cell proliferation, migration, capillary network formation, and adhesion to extracellular matrix proteins. SPRY1 knockdown was also shown to affect the expression of cyclinD1 and p21 both involved in cell-cycle regulation. These findings are discussed in relation to the role of SPRY1 as an inhibitor of ERK/MAPK signaling and to a possible explanation of its effect on cell proliferation.

conclusionsTaken together, these results suggest that SPRY1 is an endogenous angiogenesis inhibitor.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAnimalsBlotting, WesternCattleCell AdhesionCell MovementCell ProliferationCells, CulturedFemaleHCT116 CellsHumansMembrane ProteinsMiceMice, NudeNeovascularization, PathologicAdaptor Proteins, Signal TransducingMembrane ProteinsPeptide FragmentsPhosphoproteinsProlactinprolactin 16-kDa fragment, humanRNA, Small InterferingSPRY1 protein, humanSpry1 protein, mouse

Identifiers

PMID20813052
PMCPMC2944818
OpenAlexW2116263861

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.