Evidence map›Paper›PMID 34170818›Full record

ArticleeLife2021

BAP1/ASXL complex modulation regulates epithelial-mesenchymal transition during trophoblast differentiation and invasion.

Vicente Perez-Garcia, Georgia Lea, Pablo Lopez-Jimenez, Hanneke Okkenhaug, Graham J Burton, Ashley Moffett, Margherita Y Turco, Myriam Hemberger

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
12.7field-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

34 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Proteogenomic Analysis of HDAC4 and HDAC5 in Uveal Melanoma.Molecular medicine (Cambridge, Mass.) · 2026
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  13. Regulation of placental development and function by ubiquitination.Molecular medicine (Cambridge, Mass.) · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Article
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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

8 authors at 3 institutions in 3 countries.

Vicente Perez-GarciaEpigenetics Programme, The Babraham Institute, Babraham Research Campus, Cambridge, United Kingdom.ORCID https://orcid.org/0000-0001-5594-1607
Georgia LeaEpigenetics Programme, The Babraham Institute, Babraham Research Campus, Cambridge, United Kingdom.
Pablo Lopez-JimenezBiology Department, Universidad Autonoma de Madrid, Madrid, Spain.ORCID https://orcid.org/0000-0002-6673-5996
Hanneke OkkenhaugEpigenetics Programme, The Babraham Institute, Babraham Research Campus, Cambridge, United Kingdom.ORCID https://orcid.org/0000-0003-0669-4069
Graham J BurtonCentre for Trophoblast Research, Department of Physiology, Development and Neurosicence, University of Cambridge, Cambridge, United Kingdom.
Ashley MoffettCentre for Trophoblast Research, Department of Physiology, Development and Neurosicence, University of Cambridge, Cambridge, United Kingdom.
Margherita Y TurcoCentre for Trophoblast Research, Department of Physiology, Development and Neurosicence, University of Cambridge, Cambridge, United Kingdom.
Myriam HembergerEpigenetics Programme, The Babraham Institute, Babraham Research Campus, Cambridge, United Kingdom.ORCID https://orcid.org/0000-0003-3332-6958
Babraham Institute · GBUniversity of Cambridge · GBUniversidad Autónoma de Madrid · ES

Funding

Spanish Ministry of Science and Innovation RYC-2019-026956Wellcome Trust 200841/Z/16/ZWellcome Trust WT100160MA
6 · The paper itself

Abstract

Normal function of the placenta depends on the earliest developmental stages when trophoblast cells differentiate and invade into the endometrium to establish the definitive maternal-fetal interface. Previously, we identified the ubiquitously expressed tumour suppressor BRCA1-associated protein 1 (BAP1) as a central factor of a novel molecular node controlling early mouse placentation. However, functional insights into how BAP1 regulates trophoblast biology are still missing. Using CRISPR/Cas9 knockout and overexpression technology in mouse trophoblast stem cells, here we demonstrate that the downregulation of BAP1 protein is essential to trigger epithelial-mesenchymal transition (EMT) during trophoblast differentiation associated with a gain of invasiveness. Moreover, we show that the function of BAP1 in suppressing EMT progression is dependent on the binding of BAP1 to additional sex comb-like (ASXL1/2) proteins to form the polycomb repressive deubiquitinase (PR-DUB) complex. Finally, both endogenous expression patterns and BAP1 overexpression experiments in human trophoblast stem cells suggest that the molecular function of BAP1 in regulating trophoblast differentiation and EMT progression is conserved in mice and humans. Our results reveal that the physiological modulation of BAP1 determines the invasive properties of the trophoblast, delineating a new role of the BAP1 PR-DUB complex in regulating early placentation.

Indexed as

AnimalsCell DifferentiationEpithelial-Mesenchymal TransitionGene Expression RegulationHumansMiceRepressor ProteinsTrophoblastsTumor Suppressor ProteinsUbiquitin ThiolesteraseAsxl1 protein, mouseASXL2 protein, mouseBAP1 protein, humanBAP1 protein, mouseRepressor ProteinsTumor Suppressor ProteinsUbiquitin ThiolesteraseCRISPR gene editingdevelopmental biologyepithelial-mesenchymal transitionhumanmouseplacentaregenerative medicinestem cellsstem cell self-renewaltrophoblasttrophoblast invasion

Identifiers

PMID34170818
PMCPMC8233037
OpenAlexW3175501643

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.