Evidence map›Paper›PMID 26096938›Full record

ArticleOncogene2016

Translational regulation of inhibin βA by TGFβ via the RNA-binding protein hnRNP E1 enhances the invasiveness of epithelial-to-mesenchymal transitioned cells.

B V Howley, G S Hussey, L A Link, P H Howe

Abstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. INHBA: A Protein-coding Gene Closely Related to Tumour Diseases.Current topics in medicinal chemistry · 2026
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  20. Poly r(C) binding protein is post-transcriptionally repressed by MiR-490-3p to potentiate squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

4 authors at 3 institutions in 1 country.

B V HowleyDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA.
G S HusseyDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA.
L A LinkDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA.
P H HoweDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA.
Medical University of South Carolina · USKent State University · USMUSC Hollings Cancer Center · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
SC COBRE for Developmentally Based Cardiovascular DiseasesP30GM103342 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KERN, MICHAEL J · 2012 to 2016
$5.5M
Pilot and Feasibility Project ProgramP30GM103331 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KIRKWOOD, KEITH L · 2012 to 2016
$5.2M
TGF-regulated EMTR01CA154663 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Philip H Howe · 2011 to 2026
$5.1M
TRANSFORMING GROWTH FACTOR BETA SIGNALING PATHWAYSR01CA055536 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HOWE, PHILIP H · 1997 to 2017
$5.0M
NCI NIH HHS CA055536NCI NIH HHS CA154663NCI NIH HHS P30 CA138313NCI NIH HHS P30CA138313NCI NIH HHS R01 CA055536NCI NIH HHS R01 CA154663NIGMS NIH HHS P30 GM103331NIGMS NIH HHS P30GM103331NIGMS NIH HHS P30 GM103342NIGMS NIH HHS P30GM103342
6 · The paper itself

Abstract

The epithelial-to-mesenchymal transition (EMT) is a cellular process that functions during embryonic development and tissue regeneration, thought to be aberrantly activated in epithelial-derived cancer and has an important role in the process of metastasis. The transforming growth factor (TGF)-β signaling pathway is a key inducer of EMT and we have elucidated a posttranscriptional mechanism by which TGFβ modulates expression of select transcripts via the RNA-binding protein hnRNP E1 during EMT. One such transcript inhibin βA is a member of the TGFβ superfamily. Here, we show by polysome profiling that inhibin βA is translationally regulated by TGFβ via hnRNP E1. TGFβ treatment or knockdown of hnRNP E1 relieves silencing of the inhibin βA transcript, resulting in increased protein expression and secreted levels of the inhibin βA homodimer, activin A. Our data indicate that the translational upregulation of inhibin βA enhances the migration and invasion of cells that have undergone an EMT and promotes cancer progression in vivo.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCell MovementCells, CulturedDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticHeterogeneous-Nuclear RibonucleoproteinsInhibin-beta SubunitsMiceMice, Inbred C57BLMice, Inbred NODMice, SCIDMice, TransgenicNeoplasm InvasivenessProtein BiosynthesisDNA-Binding ProteinsHeterogeneous-Nuclear Ribonucleoproteinsinhibin beta A subunitInhibin-beta SubunitsPCBP1 protein, humanRNA-Binding ProteinsTransforming Growth Factor beta

Identifiers

PMID26096938
PMCPMC4688046
OpenAlexW1518912170

What OpenQuestion holds

Textmetadata
LicenceTDM
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.