Evidence map›Paper›PMID 25339690›Full record

ArticleJournal of the Royal Society, Interface2014

Towards elucidating the connection between epithelial-mesenchymal transitions and stemness.

Mohit Kumar Jolly, Bin Huang, Mingyang Lu, Sendurai A Mani, Herbert Levine, Eshel Ben-Jacob

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
8.9field-weighted citation impact, top 1% 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

106 citing papers in PubMed, 205 citations in OpenAlex.

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  4. Inflammation awakens dormant cancer cells by modulating the epithelial-mesenchymal phenotypic state.Proceedings of the National Academy of Sciences of the United States of America · 2025
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46 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

6 authors at 3 institutions in 2 countries.

Mohit Kumar JollyCenter for Theoretical Biological Physics, Rice University, Houston, TX 77005-1827, USA Department of Bioengineering, Rice University, Houston, TX 77005-1827, USA.
Bin HuangCenter for Theoretical Biological Physics, Rice University, Houston, TX 77005-1827, USA Department of Chemistry, Rice University, Houston, TX 77005-1827, USA.
Mingyang LuCenter for Theoretical Biological Physics, Rice University, Houston, TX 77005-1827, USA.
Sendurai A ManiDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA Metastasis Research Center, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Herbert LevineCenter for Theoretical Biological Physics, Rice University, Houston, TX 77005-1827, USA Department of Bioengineering, Rice University, Houston, TX 77005-1827, USA Department of Physics and Astronomy, Rice University, Houston, TX 77005-1827, USA herbert.levine@rice.edu.
Eshel Ben-JacobCenter for Theoretical Biological Physics, Rice University, Houston, TX 77005-1827, USA Department of Biosciences, Rice University, Houston, TX 77005-1827, USA School of Physics and Astronomy and The Sagol School of Neuroscience, Tel-Aviv University, Tel-Aviv 69978, Israel eshel@rice.edu.
Rice University · USCenter for Theoretical Biological Physics · USThe University of Texas MD Anderson Cancer Center · US

Funding

Pleiotropic functions of FOXC2 in EMT, stem cells and breast cancer progressionR01CA155243 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MANI, SENDURAI AYYAVOO · 2011 to 2022
$3.2M
NCI NIH HHS 5R01CA155243NCI NIH HHS R01 CA155243
6 · The paper itself

Abstract

Epithelial cells undergoing epithelial-to-mesenchymal transitions have often been shown to behave as cancer stem cells, but the precise molecular connection remains elusive. At the genetic level, stemness is governed by LIN28/let-7 double inhibition switch, whereas EMT/MET is controlled by miR-200/ZEB double inhibition circuit and LIN28 is inhibited by miR-200, coupling the two modules. Here, using a specially devised theoretical framework to investigate the dynamics of the LIN28/let-7 system, we show that it can operate as a three-way switch (between low, high and intermediate LIN28 levels termed the D, U and hybrid D/U states) similar to the three-way operation of the miR-200/ZEB circuit that allows for the existence of a hybrid epithelial/mesenchymal (E/M) phenotype. We find significant correspondence between the existence of the three states of the two circuits: E-D, M-U and E/M-D/U. Incorporating the activation of OCT4 by LIN28, we find that the hybrid E/M phenotype has high likelihood (when compared with either the E or M states) to gain stemness. Combining the LIN28/let-7 regulation by NF-κB and c-MYC, we find that NF-κB, but not c-MYC, elevates the likelihood of E/M phenotype to gain stemness. Our results are consistent with emerging concept that partial EMT can lead to stemness.

Indexed as

Epithelial-Mesenchymal TransitionModels, BiologicalHomeodomain ProteinsHumansMicroRNAsNeoplasm ProteinsNeoplasmsNeoplastic Stem CellsRNA-Binding ProteinsRNA, NeoplasmTranscription FactorsZinc Finger E-box-Binding Homeobox 1Homeodomain ProteinsLin28A protein, humanMicroRNAsMIRN200 microRNA, humanmirnlet7 microRNA, humanNeoplasm ProteinsRNA-Binding ProteinsRNA, NeoplasmTranscription FactorsZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1cancer stem cellsepithelial–mesenchymal transitionhybrid epithelial/mesenchymal phenotypeLIN28/let-7stemness

Identifiers

PMID25339690
PMCPMC4223923
OpenAlexW2043768987

What OpenQuestion holds

Textmetadata
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.