Evidence map›Paper›PMID 25502753›Full record

ArticlePloS one2014

Egr-1 activation by cancer-derived extracellular vesicles promotes endothelial cell migration via ERK1/2 and JNK signaling pathways.

Yae Jin Yoon, Dae-Kyum Kim, Chang Min Yoon, Jaesung Park, Yoon-Keun Kim, Tae-Young Roh, Yong Song Gho

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

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  8. Hitting the target: cell signaling pathways modulation by extracellular vesicles.Extracellular vesicles and circulating nucleic acids · 2024
    Review
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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

7 authors at 2 institutions in 1 country.

Yae Jin YoonDivision of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Dae-Kyum KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Chang Min YoonDepartment of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Jaesung ParkDepartment of Mechanical Engineering, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Yoon-Keun KimEwha Institute of Convergence Medicine, Ewha Womans University Medical Center, Seoul 158-710, Republic of Korea.
Tae-Young RohDivision of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea; Department of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Yong Song GhoDepartment of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Pohang University of Science and Technology · KREwha Womans University Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Various mammalian cells, including cancer cells, shed extracellular vesicles (EVs), also known as exosomes and microvesicles, into surrounding tissues. These EVs play roles in tumor growth and metastasis by promoting angiogenesis. However, the detailed mechanism of how cancer-derived EVs elicit endothelial cell activation remains unknown. Here, we provide evidence that early growth response-1 (Egr-1) activation in endothelial cells is involved in the angiogenic activity of colorectal cancer cell-derived EVs. Both RNA interference-mediated downregulation of Egr-1 and ERK1/2 or JNK inhibitor significantly blocked EV-mediated Egr-1 activation and endothelial cell migration. Furthermore, lipid raft-mediated endocytosis inhibitor effectively blocked endothelial Egr-1 activation and migration induced by cancer-derived EVs. Our results suggest that Egr-1 activation in endothelial cells may be a key mechanism involved in the angiogenic activity of cancer-derived EVs. These findings will improve our understanding regarding the proangiogenic activities of EVs in diverse pathological conditions including cancer, cardiovascular diseases, and neurodegenerative diseases.

Indexed as

MAP Kinase Signaling SystemAnimalsCell Line, TumorCell MovementEarly Growth Response Protein 1Endothelial CellsExtracellular VesiclesHCT116 CellsHumansHuman Umbilical Vein Endothelial CellsMembrane MicrodomainsMiceNeoplasmsNeovascularization, PathologicRNA InterferenceEarly Growth Response Protein 1EGR1 protein, human

Identifiers

PMID25502753
PMCPMC4264882
OpenAlexW2001665286

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.