Evidence map›Paper›PMID 31897911›Full record

ArticleAngiogenesis2020

Continuous endoglin (CD105) overexpression disrupts angiogenesis and facilitates tumor cell metastasis.

Claudia Ollauri-Ibáñez, Elena Núñez-Gómez, Cristina Egido-Turrión, Laura Silva-Sousa, Elena Díaz-Rodríguez, Alicia Rodríguez-Barbero, José M López-Novoa, Miguel Pericacho

Open access · hybridAbstract read
In one paragraph

Article in Angiogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 10% 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, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.

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  20. TGF-β superfamily co-receptors in cancer.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
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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

8 authors at 2 institutions in 1 country.

Claudia Ollauri-IbáñezRenal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, and the Biomedical Research Institute of Salamanca (IBSAL), Edificio Departamental, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
Elena Núñez-GómezRenal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, and the Biomedical Research Institute of Salamanca (IBSAL), Edificio Departamental, Campus Miguel de Unamuno, 37007, Salamanca, Spain. elena_biom2@usal.es.
Cristina Egido-TurriónRenal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, and the Biomedical Research Institute of Salamanca (IBSAL), Edificio Departamental, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
Laura Silva-SousaRenal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, and the Biomedical Research Institute of Salamanca (IBSAL), Edificio Departamental, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
Elena Díaz-RodríguezInstituto de Biología Molecular Y Celular del Cáncer. CSIC, IBSAL and CIBERONC, Salamanca, Spain.
Alicia Rodríguez-BarberoRenal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, and the Biomedical Research Institute of Salamanca (IBSAL), Edificio Departamental, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
José M López-NovoaRenal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, and the Biomedical Research Institute of Salamanca (IBSAL), Edificio Departamental, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
Miguel PericachoRenal and Cardiovascular Research Unit, Department of Physiology and Pharmacology, University of Salamanca, and the Biomedical Research Institute of Salamanca (IBSAL), Edificio Departamental, Campus Miguel de Unamuno, 37007, Salamanca, Spain. pericacho@usal.es.ORCID 0000-0003-0226-482X
Universidad de Salamanca · ESInstituto de Investigación Biomédica de Salamanca · ES

Funding

Consejería de Educación, Junta de Castilla y León GR-100Instituto de Salud Carlos III PI16/00460Instituto de Salud Carlos III RD016/0009/0025Instituto de Salud Carlos III RD06/0016/0013Instituto de Salud Carlos III RD12/0021/0032Ministerio de Economía y Competitividad SAF2010-15881Ministerio de Economía y Competitividad SAF2013-45784-R
6 · The paper itself

Abstract

Endoglin (CD105) is an auxiliary receptor for members of the TFG-β superfamily. Whereas it has been demonstrated that the deficiency of endoglin leads to minor and defective angiogenesis, little is known about the effect of its increased expression, characteristic of several types of cancer. Angiogenesis is essential for tumor growth, so high levels of proangiogenic molecules, such as endoglin, are supposed to be related to greater tumor growth leading to a poor cancer prognosis. However, we demonstrate here that endoglin overexpression do not stimulate sprouting or vascularization in several in vitro and in vivo models. Instead, steady endoglin overexpression keep endothelial cells in an active phenotype that results in an impairment of the correct stabilization of the endothelium and the recruitment of mural cells. In a context of continuous enhanced angiogenesis, such as in tumors, endoglin overexpression gives rise to altered vessels with an incomplete mural coverage that permit the extravasation of blood. Moreover, these alterations allow the intravasation of tumor cells, the subsequent development of metastases and, thus, a worse cancer prognosis.

Indexed as

AnimalsCell MovementCells, CulturedEndoglinMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsNeovascularization, PathologicUp-RegulationEndoglinEng protein, mouseAngiogenesisCancerCD105EndoglinMetastasis

Identifiers

PMID31897911
PMCPMC7160077
OpenAlexW2997471633

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.