Evidence map›Paper›PMID 31069317›Full record

ArticleAPL bioengineering2018

Interconnected feedback loops among ESRP1, HAS2, and CD44 regulate epithelial-mesenchymal plasticity in cancer.

Mohit Kumar Jolly, Bogdan-Tiberius Preca, Satyendra C Tripathi, Dongya Jia, Jason T George, Samir M Hanash, Thomas Brabletz, Marc P Stemmler, Jochen Maurer, Herbert Levine

Open access · goldAbstract read
In one paragraph

Article in APL bioengineering, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 91 citations in OpenAlex.

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  5. 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

10 authors at 1 institution in 2 countries.

Mohit Kumar JollyCenter for Theoretical Biological Physics, Rice University, Houston, Texas 77030, USA.
Bogdan-Tiberius Preca
Satyendra C TripathiDepartment of Clinical Cancer Prevention, UT MD Anderson Cancer Center, Houston, Texas 77030, USA.ORCID 0000-0003-3917-9645
Jason T George
Samir M HanashDepartment of Clinical Cancer Prevention, UT MD Anderson Cancer Center, Houston, Texas 77030, USA.
Thomas BrabletzDepartment of Experimental Medicine I, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen 91054, Germany.
Marc P StemmlerDepartment of Experimental Medicine I, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen 91054, Germany.ORCID 0000-0002-7866-3686
Herbert Levine
The University of Texas MD Anderson Cancer Center · US

Funding

Co-Evolution of the CD8+ T Cell Repertoire and AML In the Setting of ImmunotherapyF30CA213878 · NCI · RICE UNIVERSITY · PI GEORGE, JASON · 2017 to 2020
$174k
NCI NIH HHS F30 CA213878
6 · The paper itself

Abstract

Aberrant activation of epithelial-mesenchymal transition (EMT) in carcinoma cells contributes to increased migration and invasion, metastasis, drug resistance, and tumor-initiating capacity. EMT is not always a binary process; rather, cells may exhibit a hybrid epithelial/mesenchymal (E/M) phenotype. ZEB1-a key transcription factor driving EMT-can both induce and maintain a mesenchymal phenotype. Recent studies have identified two novel autocrine feedback loops utilizing epithelial splicing regulatory protein 1 (ESRP1), hyaluronic acid synthase 2 (HAS2), and CD44 which maintain high levels of ZEB1. However, how the crosstalk between these feedback loops alters the dynamics of epithelial-hybrid-mesenchymal transition remains elusive. Here, using an integrated theoretical-experimental framework, we identify that these feedback loops can enable cells to stably maintain a hybrid E/M phenotype. Moreover, computational analysis identifies the regulation of ESRP1 as a crucial node, a prediction that is validated by experiments showing that knockdown of ESRP1 in stable hybrid E/M H1975 cells drives EMT. Finally, in multiple breast cancer datasets, high levels of ESRP1, ESRP1/HAS2, and ESRP1/ZEB1 correlate with poor prognosis, supporting the relevance of ZEB1/ESRP1 and ZEB1/HAS2 axes in tumor progression. Together, our results unravel how these interconnected feedback loops act in concert to regulate ZEB1 levels and to drive the dynamics of epithelial-hybrid-mesenchymal transition.

Identifiers

PMID31069317
PMCPMC6324214
OpenAlexW2795763614

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.