Evidence map›Paper›PMID 38565950›Full record

ArticleThe EMBO journal2024

LATS1 controls CTCF chromatin occupancy and hormonal response of 3D-grown breast cancer cells.

Julieta Ramírez-Cuéllar, Roberto Ferrari, Rosario T Sanz, Marta Valverde-Santiago, Judith García-García, A Silvina Nacht, David Castillo, Francois Le Dily, Maria Victoria Neguembor, Marco Malatesta and 4 more

Open access · diamondAbstract read
In one paragraph

Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
4.2field-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

8 citing papers in PubMed, 13 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

14 authors at 6 institutions in 2 countries.

Julieta Ramírez-Cuéllar *Center for Genomic Regulation (CRG), Barcelona Institute for Science and Technology (BIST) Barcelona, Barcelona, Spain.ORCID http://orcid.org/0000-0002-9598-5222
Roberto Ferrari *Center for Genomic Regulation (CRG), Barcelona Institute for Science and Technology (BIST) Barcelona, Barcelona, Spain.ORCID http://orcid.org/0000-0002-0453-0899
Rosario T SanzMolecular Biology Institute of Barcelona, Consejo Superior de Investigaciones Científicas (IBMB-CSIC), C/ Baldiri Reixac, 4-8, 08028, Barcelona, Spain.
Marta Valverde-SantiagoMolecular Biology Institute of Barcelona, Consejo Superior de Investigaciones Científicas (IBMB-CSIC), C/ Baldiri Reixac, 4-8, 08028, Barcelona, Spain.
Judith García-GarcíaMolecular Biology Institute of Barcelona, Consejo Superior de Investigaciones Científicas (IBMB-CSIC), C/ Baldiri Reixac, 4-8, 08028, Barcelona, Spain.
A Silvina NachtCenter for Genomic Regulation (CRG), Barcelona Institute for Science and Technology (BIST) Barcelona, Barcelona, Spain.
David CastilloCNAG-CRG, Centre for Genomic Regulation, The Barcelona Institute of Science and Technology, Baldiri Reixac 4, Barcelona, 08028, Spain.
Francois Le DilyCenter for Genomic Regulation (CRG), Barcelona Institute for Science and Technology (BIST) Barcelona, Barcelona, Spain.
Maria Victoria NeguemborCenter for Genomic Regulation (CRG), Barcelona Institute for Science and Technology (BIST) Barcelona, Barcelona, Spain.ORCID http://orcid.org/0000-0002-1583-1304
Marco MalatestaDepartment of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, Parma, Italy.ORCID http://orcid.org/0000-0001-5668-0787
Sarah BonninCenter for Genomic Regulation (CRG), Barcelona Institute for Science and Technology (BIST) Barcelona, Barcelona, Spain.
Marc A Marti-RenomCenter for Genomic Regulation (CRG), Barcelona Institute for Science and Technology (BIST) Barcelona, Barcelona, Spain.
Miguel BeatoCenter for Genomic Regulation (CRG), Barcelona Institute for Science and Technology (BIST) Barcelona, Barcelona, Spain.ORCID http://orcid.org/0000-0002-2878-2222
Guillermo P VicentCenter for Genomic Regulation (CRG), Barcelona Institute for Science and Technology (BIST) Barcelona, Barcelona, Spain. gvmbmc@ibmb.csic.es.ORCID http://orcid.org/0000-0002-0554-2226
Barcelona Institute of Science and Technology · ESConsejo Superior de Investigaciones Científicas · ESUniversitat Pompeu Fabra · ESUniversity of Parma · ITCentre for Genomic Regulation · ESInstitució Catalana de Recerca i Estudis Avançats · ES

Funding

Centro de Excelencia Severo Ochoa 2013-2017EC | European Research Council (ERC) 4DGenome" nr: 609989Italian Ministry for University and Research MIUR: 2018-2022 MUR:2023-2027MEC | Consejo Superior de Investigaciones Científicas (CSIC) 201820I131Ministerio de Ciencia e Innovación (MCIN) PID2019-105173RB-I00Ministerio de Ciencia e Innovación (MCIN) PID2020-115696RB-I00Ministerio de Ciencia e Innovación (MCIN) PID2022-137045OB-I00
6 · The paper itself

Abstract

The cancer epigenome has been studied in cells cultured in two-dimensional (2D) monolayers, but recent studies highlight the impact of the extracellular matrix and the three-dimensional (3D) environment on multiple cellular functions. Here, we report the physical, biochemical, and genomic differences between T47D breast cancer cells cultured in 2D and as 3D spheroids. Cells within 3D spheroids exhibit a rounder nucleus with less accessible, more compacted chromatin, as well as altered expression of ~2000 genes, the majority of which become repressed. Hi-C analysis reveals that cells in 3D are enriched for regions belonging to the B compartment, have decreased chromatin-bound CTCF and increased fusion of topologically associating domains (TADs). Upregulation of the Hippo pathway in 3D spheroids results in the activation of the LATS1 kinase, which promotes phosphorylation and displacement of CTCF from DNA, thereby likely causing the observed TAD fusions. 3D cells show higher chromatin binding of progesterone receptor (PR), leading to an increase in the number of hormone-regulated genes. This effect is in part mediated by LATS1 activation, which favors cytoplasmic retention of YAP and CTCF removal.

Indexed as

Breast NeoplasmsCCCTC-Binding FactorChromatinProtein Serine-Threonine KinasesCell Line, TumorFemaleGene Expression Regulation, NeoplasticHippo Signaling PathwayHumansReceptors, ProgesteroneSpheroids, CellularCCCTC-Binding FactorChromatinCTCF protein, humanLATS1 protein, humanProtein Serine-Threonine KinasesReceptors, ProgesteroneBreast CancerCTCFLATS1 Kinase and Hormonal ResponseThree-dimensional Cell Growth

Identifiers

PMID38565950
PMCPMC11066098
OpenAlexW4393396956

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.