Evidence map›Paper›PMID 33772115›Full record

ArticleCommunications biology2021

CENP-A overexpression promotes distinct fates in human cells, depending on p53 status.

Daniel Jeffery, Alberto Gatto, Katrina Podsypanina, Charlène Renaud-Pageot, Rebeca Ponce Landete, Lorraine Bonneville, Marie Dumont, Daniele Fachinetti, Geneviève Almouzni

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Daniel JefferyInstitut Curie, PSL Research University, CNRS, Sorbonne Université, Nuclear Dynamics Unit, Equipe Labellisée Ligue contre le Cancer, Paris, France.ORCID 0000-0003-2289-8379
Alberto GattoInstitut Curie, PSL Research University, CNRS, Sorbonne Université, Nuclear Dynamics Unit, Equipe Labellisée Ligue contre le Cancer, Paris, France.ORCID 0000-0002-8378-0131
Katrina PodsypaninaInstitut Curie, PSL Research University, CNRS, Sorbonne Université, Nuclear Dynamics Unit, Equipe Labellisée Ligue contre le Cancer, Paris, France.
Charlène Renaud-PageotInstitut Curie, PSL Research University, CNRS, Sorbonne Université, Nuclear Dynamics Unit, Equipe Labellisée Ligue contre le Cancer, Paris, France.ORCID 0000-0001-6926-6825
Rebeca Ponce LandeteInstitut Curie, PSL Research University, CNRS, Sorbonne Université, Nuclear Dynamics Unit, Equipe Labellisée Ligue contre le Cancer, Paris, France.ORCID 0000-0001-6933-4365
Lorraine BonnevilleInstitut Curie, PSL Research University, CNRS, Sorbonne Université, Nuclear Dynamics Unit, Equipe Labellisée Ligue contre le Cancer, Paris, France.
Marie DumontInstitut Curie, PSL Research University, Centre de Recherche, Sorbonne Université, Cell Biology and Cancer Unit, Paris, France.
Daniele FachinettiInstitut Curie, PSL Research University, Centre de Recherche, Sorbonne Université, Cell Biology and Cancer Unit, Paris, France.ORCID 0000-0002-8795-6771
Geneviève AlmouzniInstitut Curie, PSL Research University, CNRS, Sorbonne Université, Nuclear Dynamics Unit, Equipe Labellisée Ligue contre le Cancer, Paris, France. genevieve.almouzni@curie.fr.ORCID 0000-0001-5570-0723
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour evolution is driven by both genetic and epigenetic changes. CENP-A, the centromeric histone H3 variant, is an epigenetic mark that directly perturbs genetic stability and chromatin when overexpressed. Although CENP-A overexpression is a common feature of many cancers, how this impacts cell fate and response to therapy remains unclear. Here, we established a tunable system of inducible and reversible CENP-A overexpression combined with a switch in p53 status in human cell lines. Through clonogenic survival assays, single-cell RNA-sequencing and cell trajectory analysis, we uncover the tumour suppressor p53 as a key determinant of how CENP-A impacts cell state, cell identity and therapeutic response. If p53 is functional, CENP-A overexpression promotes senescence and radiosensitivity. Surprisingly, when we inactivate p53, CENP-A overexpression instead promotes epithelial-mesenchymal transition, an essential process in mammalian development but also a precursor for tumour cell invasion and metastasis. Thus, we uncover an unanticipated function of CENP-A overexpression to promote cell fate reprogramming, with important implications for development and tumour evolution.

Indexed as

Gene Expression RegulationCentromere Protein AHumansRNA-SeqSingle-Cell AnalysisTumor Suppressor Protein p53Centromere Protein ATP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID33772115
PMCPMC7997993
OpenAlexW3139454364

What OpenQuestion holds

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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.