Evidence map›Paper›PMID 25636082›Full record

ArticleNature communications2015

NR2F1 controls tumour cell dormancy via SOX9- and RARβ-driven quiescence programmes.

Maria Soledad Sosa, Falguni Parikh, Alexandre Gaspar Maia, Yeriel Estrada, Almudena Bosch, Paloma Bragado, Esther Ekpin, Ajish George, Yang Zheng, Hung-Ming Lam and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 256 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
256citing papers in PubMed, 2 pooled it
9.3field-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

256 citing papers in PubMed, 2 syntheses or guidelines pooled it, 336 citations in OpenAlex.

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196 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

15 authors at 2 institutions in 1 country.

Maria Soledad SosaDivision of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
Falguni Parikh1] Division of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA [2] Department of Otolaryngology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Alexandre Gaspar MaiaDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA.
Yeriel EstradaDivision of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
Almudena BoschDivision of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
Paloma BragadoDivision of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
Esther EkpinDivision of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
Ajish GeorgeDivision of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
Yang ZhengDepartment of Otolaryngology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Hung-Ming LamDepartment of Urology, University of Washington, Seattle, Washington, WA 98195, USA.
Colm MorrisseyDepartment of Urology, University of Washington, Seattle, Washington, WA 98195, USA.
Chi-Yeh ChungDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA.
Eduardo F Farias1] Division of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA [2] Tisch Cancer Institute, Mount Sinai School of Medicine, New York, New York 10029, USA.
Emily Bernstein1] Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA [2] Tisch Cancer Institute, Mount Sinai School of Medicine, New York, New York 10029, USA [3] Black Family Stem Cell Institute, Mount Sinai School of Medicine, New York, New York 10029, USA.
Julio A Aguirre-Ghiso1] Division of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA [2] Department of Otolaryngology, Mount Sinai School of Medicine, New York, New York 10029, USA [3] Tisch Cancer Institute, Mount Sinai School of Medicine, New York, New York 10029, USA [4] Black Family Stem Cell Institute, Mount Sinai School of Medicine, New York, New York 10029, USA.
Icahn School of Medicine at Mount Sinai · USUniversity of Washington · US

Funding

Functional Determinants of Metastatic DormancyR01CA109182 · NCI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI AGUIRRE-GHISO, JULIO A. · 2005 to 2025
$8.3M
Tumor microenvironments determing migration, dissemination and dormancyU54CA163131 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI AGUIRRE-GHISO, JULIO A., CASTRACANE, JAMES · 2011 to 2015
$3.9M
Profiling and Characterizing Prostate Cancer Tumor Dormancy in the Bone MarrowRC1CA144825 · NCI · UNIVERSITY OF WASHINGTON · PI VESSELLA, ROBERT LOUIS · 2009 to 2010
$999k
Translational Machinery in Stress Signaling and Tumor SuppressionR21ES017146 · NIEHS · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI AGUIRRE-GHISO, JULIO A., BEGLEY, THOMAS J · 2009 to 2010
$454k
NCI NIH HHS CA109182NCI NIH HHS CA163131NCI NIH HHS R01 CA109182NCI NIH HHS RC1 CA144825NCI NIH HHS RC1 CA144825-0NCI NIH HHS U54 CA163131NIEHS NIH HHS ES017146NIEHS NIH HHS R21 ES017146
6 · The paper itself

Abstract

Metastases can originate from disseminated tumour cells (DTCs), which may be dormant for years before reactivation. Here we find that the orphan nuclear receptor NR2F1 is epigenetically upregulated in experimental head and neck squamous cell carcinoma (HNSCC) dormancy models and in DTCs from prostate cancer patients carrying dormant disease for 7-18 years. NR2F1-dependent dormancy is recapitulated by a co-treatment with the DNA-demethylating agent 5-Aza-C and retinoic acid across various cancer types. NR2F1-induced quiescence is dependent on SOX9, RARβ and CDK inhibitors. Intriguingly, NR2F1 induces global chromatin repression and the pluripotency gene NANOG, which contributes to dormancy of DTCs in the bone marrow. When NR2F1 is blocked in vivo, growth arrest or survival of dormant DTCs is interrupted in different organs. We conclude that NR2F1 is a critical node in dormancy induction and maintenance by integrating epigenetic programmes of quiescence and survival in DTCs.

Indexed as

AnimalsCell Line, TumorCOUP Transcription Factor IFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansImmunohistochemistryMaleMiceMice, NudeProstatic NeoplasmsReceptors, Retinoic AcidRNA InterferenceSOX9 Transcription FactorTumor Cells, CulturedCOUP Transcription Factor IHomeodomain ProteinsReceptors, Retinoic AcidSOX9 Transcription Factor

Identifiers

PMID25636082
PMCPMC4313575
OpenAlexW2115900736

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.