Evidence map›Paper›PMID 30405106›Full record

ArticleNature communications2018

Genetic dissection of the miR-200-Zeb1 axis reveals its importance in tumor differentiation and invasion.

Alexandra C Title, Sue-Jean Hong, Nuno D Pires, Lynn Hasenöhrl, Svenja Godbersen, Nadine Stokar-Regenscheit, David P Bartel, Markus Stoffel

Abstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
–field-weighted citation impact
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

74 citing papers in PubMed.

  1. Role of ZEB1 in angiogenesis and therapeutic potential (Review).International journal of molecular medicine · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. ZEB1 and Uveal Melanoma Invasiveness.International journal of molecular sciences · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Zeb1 and Tle3 are trans-factors that differentially regulate the expression of myosin heavy chain-embryonic and skeletal muscle differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  19. Article
  20. Article

14 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

8 authors.

Alexandra C TitleInstitute of Molecular Health Sciences, ETH Zurich, Otto-Stern-Weg 7, 8093, Zürich, Switzerland.
Sue-Jean HongHoward Hughes Medical Institute and Whitehead Institute for Biomedical Research, Cambridge, MA, 02142, USA.
Nuno D PiresInstitute of Molecular Health Sciences, ETH Zurich, Otto-Stern-Weg 7, 8093, Zürich, Switzerland.
Lynn HasenöhrlInstitute of Molecular Health Sciences, ETH Zurich, Otto-Stern-Weg 7, 8093, Zürich, Switzerland.
Svenja GodbersenInstitute of Molecular Health Sciences, ETH Zurich, Otto-Stern-Weg 7, 8093, Zürich, Switzerland.
Nadine Stokar-RegenscheitInstitute of Animal Pathology (COMPATH), Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland.
David P BartelHoward Hughes Medical Institute and Whitehead Institute for Biomedical Research, Cambridge, MA, 02142, USA.
Markus StoffelInstitute of Molecular Health Sciences, ETH Zurich, Otto-Stern-Weg 7, 8093, Zürich, Switzerland. stoffel@biol.ethz.ch.

Funding

Post-transcriptional gene regulationR35GM118135 · NIGMS · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI DAVID P BARTEL · 2016 to 2026
$10.7M
NIGMS NIH HHS R35 GM118135
6 · The paper itself

Abstract

The epithelial-to-mesenchymal transition (EMT) is an important mechanism for cancer progression and metastasis. Numerous in vitro and tumor-profiling studies point to the miR-200-Zeb1 axis as crucial in regulating this process, yet in vivo studies involving its regulation within a physiological context are lacking. Here, we show that miR-200 ablation in the Rip-Tag2 insulinoma mouse model induces beta-cell dedifferentiation, initiates an EMT expression program, and promotes tumor invasion. Strikingly, disrupting the miR-200 sites of the endogenous Zeb1 locus causes a similar phenotype. Reexpressing members of the miR-200 superfamily in vitro reveals that the miR-200c family and not the co-expressed and closely related miR-141 family is responsible for regulation of Zeb1 and EMT. Our results thus show that disrupting the in vivo regulation of Zeb1 by miR-200c is sufficient to drive EMT, thus highlighting the importance of this axis in tumor progression and invasion and its potential as a therapeutic target.

Indexed as

Cell DifferentiationSignal TransductionAnimalsBase SequenceCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGene Regulatory NetworksMice, Inbred C57BLMicroRNAsMutationNeoplasm InvasivenessNeoplasmsZinc Finger E-box-Binding Homeobox 1MicroRNAsMirn141 microRNA, mouseMirn200 microRNA, mouseZEB1 protein, mouseZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID30405106
PMCPMC6220299

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.