Evidence map›Paper›PMID 25023702›Full record

ArticleOncogene2015

EFNA3 long noncoding RNAs induced by hypoxia promote metastatic dissemination.

L Gómez-Maldonado, M Tiana, O Roche, A Prado-Cabrero, L Jensen, A Fernandez-Barral, I Guijarro-Muñoz, E Favaro, G Moreno-Bueno, L Sanz and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

72 citing papers in PubMed, 116 citations in OpenAlex.

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  17. Key events in cancer: Dysregulation of SREBPs.Frontiers in pharmacology · 2023
    Review
  18. Hypoxia-driven ncRNAs in breast cancer.Frontiers in oncology · 2023
    Review
  19. Review
  20. Review

12 more citing papers are in PubMed but not listed here.

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

15 authors at 7 institutions in 4 countries.

L Gómez-MaldonadoDepartamento de Bioquímica, Universidad Autónoma de Madrid (UAM) and Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Madrid, Spain.
M TianaDepartamento de Bioquímica, Universidad Autónoma de Madrid (UAM) and Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Madrid, Spain.
O Roche1] Departamento de Bioquímica, Universidad Autónoma de Madrid (UAM) and Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Madrid, Spain [2] IdiPaz, Instituto de Investigación Sanitaria del Hospital Universitario La Paz, Madrid, Spain.
A Prado-CabreroDepartamento de Bioquímica, Universidad Autónoma de Madrid (UAM) and Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Madrid, Spain.
L Jensen1] Department of Medicine and Health Sciences, Linköping University Linköping, Sweden [2] Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, Stockholm, Sweden.
A Fernandez-BarralDepartamento de Bioquímica, Universidad Autónoma de Madrid (UAM) and Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Madrid, Spain.
I Guijarro-MuñozMolecular Immunology Unit, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.
E FavaroMolecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.
G Moreno-BuenoDepartamento de Bioquímica, Universidad Autónoma de Madrid (UAM) and Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Madrid, Spain.
L SanzMolecular Immunology Unit, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.
J AragonesResearch Unit, Hospital Universitario Santa Cristina, Research Institute Princesa, Autonomous University of Madrid, Madrid, Spain.
A HarrisMolecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.
O VolpertUrology Department, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
B JimenezDepartamento de Bioquímica, Universidad Autónoma de Madrid (UAM) and Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Madrid, Spain.
L del Peso1] Departamento de Bioquímica, Universidad Autónoma de Madrid (UAM) and Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Madrid, Spain [2] IdiPaz, Instituto de Investigación Sanitaria del Hospital Universitario La Paz, Madrid, Spain.ORCID 0000000340145688
Instituto de Investigaciones Biomédicas Sols-Morreale · ESHospital Universitario Puerta de Hierro Majadahonda · ESJohn Radcliffe Hospital · GBHospital Universitario La Paz · ESHospital Universitario Santa Cristina · ESLinköping University · SENorthwestern University · US

Funding

Apigenin restores TSP-1 expression in UVB-irradiated keratinocytesR01CA172669 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI VOLPERT, OLGA VALERY · 2013 to 2017
$2.3M
Cancer Research UK 11359Cancer Research UK 16466Cancer Research UK 18974NCI NIH HHS R01 CA172669
6 · The paper itself

Abstract

The presence of hypoxic regions in solid tumors is an adverse prognostic factor for patient outcome. Here, we show that hypoxia induces the expression of Ephrin-A3 through a novel hypoxia-inducible factor (HIF)-mediated mechanism. In response to hypoxia, the coding EFNA3 mRNA levels remained relatively stable, but HIFs drove the expression of previously unknown long noncoding (lnc) RNAs from EFNA3 locus and these lncRNA caused Ephrin-A3 protein accumulation. Ephrins are cell surface proteins that regulate diverse biological processes by modulating cellular adhesion and repulsion. Mounting evidence implicates deregulated ephrin function in multiple aspects of tumor biology. We demonstrate that sustained expression of both Ephrin-A3 and novel EFNA3 lncRNAs increased the metastatic potential of human breast cancer cells, possibly by increasing the ability of tumor cells to extravasate from the blood vessels into surrounding tissue. In agreement, we found a strong correlation between high EFNA3 expression and shorter metastasis-free survival in breast cancer patients. Taken together, our results suggest that hypoxia could contribute to metastatic spread of breast cancer via HIF-mediated induction of EFNA3 lncRNAs and subsequent Ephrin-A3 protein accumulation.

Indexed as

Genetic LociAnimalsBreast NeoplasmsCell HypoxiaCell Line, TumorEphrin-A3FemaleHumansHuman Umbilical Vein Endothelial CellsHypoxia-Inducible Factor 1MiceMice, NudeNeoplasm MetastasisNeoplasm ProteinsRNA, Long NoncodingRNA, NeoplasmEphrin-A3Hypoxia-Inducible Factor 1Neoplasm ProteinsRNA, Long NoncodingRNA, Neoplasm

Identifiers

PMID25023702
PMCPMC4722872
OpenAlexW2026209030

What OpenQuestion holds

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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.