Evidence map›Paper›PMID 38786098›Full record

ArticleCells2024

PI 3-Kinase and the Histone Methyl-Transferase KMT2D Collaborate to Induce Arp2/3-Dependent Migration of Mammary Epithelial Cells.

Karina D Rysenkova, Julia Gaboriaud, Artem I Fokin, Raphaëlle Toubiana, Alexandre Bense, Camil Mirdass, Mélissa Jin, Minh Chau N Ho, Elizabeth Glading, Sophie Vacher and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Karina D RysenkovaLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.ORCID 0000-0003-1325-4002
Julia GaboriaudLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.ORCID 0009-0005-9581-3251
Artem I FokinLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.ORCID 0000-0003-2205-8441
Raphaëlle ToubianaLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.
Alexandre BenseLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.
Camil MirdassLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.
Mélissa JinLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.
Minh Chau N HoLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.
Elizabeth GladingLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.
Sophie VacherPharmacogenomics Unit, Department of Genetics, Institut Curie, Paris Descartes University, 75005 Paris, France.ORCID 0000-0002-0042-6023
Laura CourtoisPharmacogenomics Unit, Department of Genetics, Institut Curie, Paris Descartes University, 75005 Paris, France.
Ivan BièchePharmacogenomics Unit, Department of Genetics, Institut Curie, Paris Descartes University, 75005 Paris, France.
Alexis M GautreauLaboratoire de Biologie Structurale de la Cellule, CNRS UMR7654, Ecole Polytechnique, Institut Polytechnique de Paris, 91128 Palaiseau Cedex, France.ORCID 0000-0002-2369-4362

Funding

Agence Nationale de la Recherche ANR-20-CE13-0016Agence Nationale de la Recherche ANR-22-CE13-0041Fondation ARC pour la Recherche sur le Cancer ARCPDF12020080002578Fondation ARC pour la Recherche sur le Cancer ARC PJA 2021 060003815French National Cancer Institute INCA_11508French National Cancer Institute INCA_16712
6 · The paper itself

Abstract

Breast cancer develops upon sequential acquisition of driver mutations in mammary epithelial cells; however, how these mutations collaborate to transform normal cells remains unclear in most cases. We aimed to reconstitute this process in a particular case. To this end, we combined the activated form of the PI 3-kinase harboring the H1047R mutation with the inactivation of the histone lysine methyl-transferase KMT2D in the non-tumorigenic human mammary epithelial cell line MCF10A. We found that PI 3-kinase activation promoted cell-cycle progression, especially when growth signals were limiting, as well as cell migration, both in a collective monolayer and as single cells. Furthermore, we showed that KMT2D inactivation had relatively little influence on these processes, except for single-cell migration, which KMT2D inactivation promoted in synergy with PI 3-kinase activation. The combination of these two genetic alterations induced expression of the

Indexed as

Actin-Related Protein 2-3 ComplexCell MovementEpithelial CellsHistone-Lysine N-MethyltransferasePhosphatidylinositol 3-KinasesCell LineDNA-Binding ProteinsFemaleHumansMammary Glands, HumanMutationNeoplasm ProteinsActin-Related Protein 2-3 ComplexDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseKMT2D protein, humanNeoplasm ProteinsPhosphatidylinositol 3-KinasesArp2/3KMT2DMLL2MLL4PIK3CA

Identifiers

PMID38786098
PMCPMC11119607

What OpenQuestion holds

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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.