Evidence map›Paper›PMID 23951165›Full record

ArticlePloS one2013

EphA2-induced angiogenesis in ewing sarcoma cells works through bFGF production and is dependent on caveolin-1.

Miguel Sáinz-Jaspeado, Juan Huertas-Martinez, Laura Lagares-Tena, Juan Martin Liberal, Silvia Mateo-Lozano, Enrique de Alava, Carmen de Torres, Jaume Mora, Xavier Garcia Del Muro, Oscar M Tirado

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Cellular crosstalk in the bone marrow niche.Journal of translational medicine · 2024
    Review
  4. EphA2 in Cancer: Molecular Complexity and Therapeutic Opportunities.International journal of molecular sciences · 2024
    Review
  5. Targeting the EphA2 pathway: could it be the way for bone sarcomas?Cell communication and signaling : CCS · 2024
    Review
  6. Deciphering the code: Advancing therapies for endometriosis and cancer with DNA-encoded drug discovery.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Identification of potent pan-ephrin receptor kinase inhibitors using DNA-encoded chemistry technology.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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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 at 4 institutions in 1 country.

Miguel Sáinz-JaspeadoSarcoma Research Group, Laboratori d'Oncología Molecular, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain.
Juan Huertas-Martinez
Laura Lagares-Tena
Juan Martin Liberal
Silvia Mateo-Lozano
Enrique de Alava
Carmen de Torres
Jaume Mora
Xavier Garcia Del Muro
Oscar M Tirado
Institut d'Investigació Biomédica de Bellvitge · ESHospital Sant Joan de Déu Barcelona · ESCIBBIM-Nanomedicine · ESUniversidad de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is the result of the combined activity of the tumor microenvironment and signaling molecules. The angiogenic switch is represented as an imbalance between pro- and anti-angiogenic factors and is a rate-limiting step in the development of tumors. Eph receptor tyrosine kinases and their membrane-anchored ligands, known as ephrins, constitute the largest receptor tyrosine kinase (RTK) subfamily and are considered a major family of pro-angiogenic RTKs. Ewing sarcoma (EWS) is a highly aggressive bone and soft tissue tumor affecting children and young adults. As other solid tumors, EWS are reliant on a functional vascular network for the delivery of nutrients and oxygen and for the removal of waste. Based on the biological roles of EphA2 in promoting angiogenesis, we explored the functional role of this receptor and its relationship with caveolin-1 (CAV1) in EWS angiogenesis. We demonstrated that lack of CAV1 results in a significant reduction in micro vascular density (MVD) on 3 different in vivo models. In vitro, this phenomenon correlated with inactivation of EphA2 receptor, lack of AKT response and downregulation of bFGF. We also demonstrated that secreted bFGF from EWS cells acted as chemoattractant for endothelial cells. Furthermore, interaction between EphA2 and CAV1 was necessary for the right localization and signaling of the receptor to produce bFGF through AKT and promote migration of endothelial cells. Finally, introduction of a dominant-negative form of EphA2 into EWS cells mostly reproduced the effects occurred by CAV1 silencing, strongly suggesting that the axis EphA2-CAV1 participates in the promotion of endothelial cell migration toward the tumors favoring EWS angiogenesis.

Indexed as

AnimalsBone NeoplasmsCaveolin 1Cell Line, TumorCell MovementDisease Models, AnimalEndothelial CellsFemaleFibroblast Growth Factor 2Gene SilencingHeterograftsHumansMiceMice, KnockoutNeovascularization, PathologicProtein BindingCaveolin 1Fibroblast Growth Factor 2Proto-Oncogene Proteins c-aktReceptor, EphA2

Identifiers

PMID23951165
PMCPMC3741133
OpenAlexW1970399172

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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.