Evidence map›Paper›PMID 35021086›Full record

ArticleCell reports2022

Coordinate control of basal epithelial cell fate and stem cell maintenance by core EMT transcription factor Zeb1.

Yingying Han, Alvaro Villarreal-Ponce, Guadalupe Gutierrez, Quy Nguyen, Peng Sun, Ting Wu, Benjamin Sui, Geert Berx, Thomas Brabletz, Kai Kessenbrock and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.1field-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

26 citing papers in PubMed, 38 citations in OpenAlex.

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  8. Mechanisms of Regulation of Cell Fate in Breast Development and Cancer.Advances in experimental medicine and biology · 2025
    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

13 authors at 4 institutions in 5 countries.

Yingying HanDepartment of Biological Chemistry, School of Medicine, D250 Med Sci I, University of California, Irvine, Irvine, CA 92697-1700, USA.
Alvaro Villarreal-PonceDepartment of Biological Chemistry, School of Medicine, D250 Med Sci I, University of California, Irvine, Irvine, CA 92697-1700, USA.
Guadalupe GutierrezDepartment of Biological Chemistry, School of Medicine, D250 Med Sci I, University of California, Irvine, Irvine, CA 92697-1700, USA.
Quy NguyenDepartment of Biological Chemistry, School of Medicine, D250 Med Sci I, University of California, Irvine, Irvine, CA 92697-1700, USA.
Peng SunDepartment of Biological Chemistry, School of Medicine, D250 Med Sci I, University of California, Irvine, Irvine, CA 92697-1700, USA.
Ting WuInstitute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue-yang Road, Shanghai 200031, China.
Benjamin SuiDepartment of Biological Chemistry, School of Medicine, D250 Med Sci I, University of California, Irvine, Irvine, CA 92697-1700, USA.
Geert BerxMolecular and Cellular Oncology Lab, Department of Biomedical Molecular Biology, Ghent University, Technologiepark 71, 9052 Zwijnaarde, Belgium; Cancer Research Institute Ghent, Ghent, Belgium.
Thomas BrabletzDepartment of Experimental Medicine, Nikolaus-Fiebiger-Center for Molecular Medicine I, University, Erlangen-Nuernberg Glueckstr. 6, 91054 Erlangen, Germany.
Kai KessenbrockDepartment of Biological Chemistry, School of Medicine, D250 Med Sci I, University of California, Irvine, Irvine, CA 92697-1700, USA.
Yi Arial ZengInstitute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue-yang Road, Shanghai 200031, China.
Kazuhide WatanabeDepartment of Biological Chemistry, School of Medicine, D250 Med Sci I, University of California, Irvine, Irvine, CA 92697-1700, USA; RIKEN Center for Integrative Medical Sciences, Yokohama 230-0045, Japan.
Xing DaiDepartment of Biological Chemistry, School of Medicine, D250 Med Sci I, University of California, Irvine, Irvine, CA 92697-1700, USA. Electronic address: xdai@uci.edu.
University of California, Irvine · USChinese Academy of Sciences · CNFriedrich-Alexander-Universität Erlangen-Nürnberg · DEGhent University · BE

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Christine Hui · 1994 to 2026
$57.9M
UCI P30 Skin Center Systems Biology CoreP30AR075047 · NIAMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI ANDERSEN, BOGI, GANESAN, ANAND K · 2019 to 2025
$5.1M
Multiscale Models of Wound Cell Plasticity for RegenerationU01AR073159 · NIAMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI DAI, XING, NIE, QING · 2018 to 2022
$3.5M
Intrinsic and extrinsic control of epithelial tissue stem cell activityR35GM145307 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Xing Dai · 2022 to 2026
$2.2M
Mammary basal/stem cell plasticity and regulationR01GM123731 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI DAI, XING · 2017 to 2020
$1.9M
Control of epithelial plasticity and differentiation in hair follicle stem/progenitor cellsR01AR068074 · NIAMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI DAI, XING · 2015 to 2019
$1.7M
NCI NIH HHS P30 CA062203NIAMS NIH HHS P30 AR075047NIAMS NIH HHS R01 AR068074NIAMS NIH HHS U01 AR073159NIGMS NIH HHS R01 GM123731NIGMS NIH HHS R35 GM145307
6 · The paper itself

Abstract

Maintenance of undifferentiated, long-lived, and often quiescent stem cells in the basal compartment is important for homeostasis and regeneration of multiple epithelial tissues, but the molecular mechanisms that coordinately control basal cell fate and stem cell quiescence are elusive. Here, we report an epithelium-intrinsic requirement for Zeb1, a core transcriptional inducer of epithelial-to-mesenchymal transition, for mammary epithelial ductal side branching and for basal cell regenerative capacity. Our findings uncover an evolutionarily conserved role of Zeb1 in promoting basal cell fate over luminal differentiation. We show that Zeb1 loss results in increased basal cell proliferation at the expense of quiescence and self-renewal. Moreover, Zeb1 cooperates with YAP to activate Axin2 expression, and inhibition of Wnt signaling partially restores stem cell function to Zeb1-deficient basal cells. Thus, Zeb1 is a transcriptional regulator that maintains both basal cell fate and stem cell quiescence, and it functions in part through suppressing Wnt signaling.

Indexed as

3T3 CellsAnimalsAxin ProteinCell DifferentiationCell LineageCell ProliferationEpithelial CellsEpithelial-Mesenchymal TransitionHEK293 CellsHumansMiceMice, Inbred C57BLStem CellsTranscription FactorsWnt Signaling PathwayZinc Finger E-box-Binding Homeobox 1Axin2 protein, mouseAxin ProteinTranscription FactorsZEB1 protein, mouseZinc Finger E-box-Binding Homeobox 1Axin2basal stem cellEMTepithelial-mesenchymal transitionmammary glandOvol2quiescenceWnt signalingZeb1

Identifiers

PMID35021086
PMCPMC9894649
OpenAlexW4205583335

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.