Evidence map›Paper›PMID 25980435›Full record

ArticleOncotarget2015

YBX1/YB-1 induces partial EMT and tumourigenicity through secretion of angiogenic factors into the extracellular microenvironment.

Shashi K Gopal, David W Greening, Rommel A Mathias, Hong Ji, Alin Rai, Maoshan Chen, Hong-Jian Zhu, Richard J Simpson

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 72 citations in OpenAlex.

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  7. Cancer spreading patterns based on epithelial-mesenchymal plasticity.Frontiers in cell and developmental biology · 2024
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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.

Shashi K GopalDepartment of Molecular Science, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria, Australia.
David W GreeningDepartment of Molecular Science, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria, Australia.
Rommel A MathiasDepartment of Molecular Science, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria, Australia.
Hong JiDepartment of Molecular Science, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria, Australia.
Alin RaiDepartment of Molecular Science, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria, Australia.
Maoshan ChenDepartment of Molecular Science, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria, Australia.
Hong-Jian ZhuDepartment of Surgery, The University of Melbourne, Melbourne, Victoria, Australia.
Richard J SimpsonDepartment of Molecular Science, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria, Australia.
La Trobe University · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) describes a morphogenetic program which confers mesenchymal cell properties, such as reduced cell-cell contact and increased cell migration and invasion, to epithelial cells. Here we investigate the role of the pleiotropic transcription/splicing factor and RNA-binding protein nuclease-sensitive element-binding protein 1 (YBX1/YB-1) in increasing the oncogenic potential of epithelial MDCK cells. Characterization of MDCK cells expressing YBX1 (MDCKYBX1 cells) revealed a partial EMT phenotype, including cytosolic relocalization of E-cadherin, increased cell scattering, and anchorage-independent growth. Subcutaneous injection of parental MDCK cells into NOD/SCID mice did not form tumours. Critically, MDCKYBX1 cells established viable tumour xenografts, and immuno-histochemical staining indicated murine vascularization by CD31+ endothelial cells. We analysed the total secretome (containing soluble and extracellular vesicles) of MDCKYBX1 cells to investigate regulation of the tumour microenvironment. YBX1 expression elevated release of secreted factors known to enhance angiogenesis (TGF-β, CSF-1, NGF, VGF, ADAM9 and ADAM17), compared to MDCK cells. Importantly, treatment with MDCKYBX1 cell-derived secretome increased recipient 2F-2B endothelial cell motility. This defines YBX1 as an oncogenic enhancer that can regulate tumour angiogenesis via release of secreted modulators into the extracellular microenvironment.

Indexed as

Angiogenesis Inducing AgentsAnimalsCell MovementDogsEpithelial-Mesenchymal TransitionMadin Darby Canine Kidney CellsMaleMiceMice, Inbred NODMice, SCIDNeovascularization, PathologicTumor MicroenvironmentXenograft Model Antitumor AssaysY-Box-Binding Protein 1Angiogenesis Inducing AgentsY-Box-Binding Protein 1EMTepithelial-mesenchymal transitionsecretometumorigenesisYBX1

Identifiers

PMID25980435
PMCPMC4537044
OpenAlexW1537016873

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.