Evidence map›Paper›PMID 26807845›Full record

ArticlePLoS genetics2016

Post-transcriptional Control of Tumor Cell Autonomous Metastatic Potential by CCR4-NOT Deadenylase CNOT7.

Farhoud Faraji, Ying Hu, Howard H Yang, Maxwell P Lee, G Sebastian Winkler, Markus Hafner, Kent W Hunter

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

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  10. SMARCD1 is a "Goldilocks" metastasis modifier.bioRxiv : the preprint server for biology · 2024
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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

7 authors at 4 institutions in 2 countries.

Farhoud FarajiMetastasis Susceptibility Section, Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Ying HuCenter for Biomedical Informatics and Information Technology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Howard H YangMetastasis Susceptibility Section, Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Maxwell P LeeMetastasis Susceptibility Section, Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
G Sebastian WinklerSchool of Pharmacy, University of Nottingham, Nottingham, United Kingdom.
Markus HafnerLaboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Kent W HunterMetastasis Susceptibility Section, Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
National Institutes of Health · USNational Cancer Institute · USCenter for Cancer Research · USUniversity of Nottingham · GB

Funding

Genetic Modifiers of Intitiation and Progression of Mammary CancerZIABC011255 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HUNTER, KENT WILLIAM · 2010 to 2025
$33.2M
Integrated analyses of genetics, epigenetics, and gene expressionZIHBC011703 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LEE, MAXWELL · 2016 to 2025
$10.9M
Integration of the results from systems-level determination of cis-acting elements into high-resolution maps of posttranscriptional regulatory events.ZIAAR041205 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI HAFNER, MARKUS · 2016 to 2025
$5.5M
The role of AU-rich element binding proteins in shaping target mRNA expressionZIAAR041200 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI HAFNER, MARKUS · 2014 to 2023
$5.1M
Biotechnology and Biological Sciences Research Council BB/E02338X/1Intramural NIH HHSWorldwide Cancer Research 07-0494
6 · The paper itself

Abstract

Accumulating evidence supports the role of an aberrant transcriptome as a driver of metastatic potential. Deadenylation is a general regulatory node for post-transcriptional control by microRNAs and other determinants of RNA stability. Previously, we demonstrated that the CCR4-NOT scaffold component Cnot2 is an inherited metastasis susceptibility gene. In this study, using orthotopic metastasis assays and genetically engineered mouse models, we show that one of the enzymatic subunits of the CCR4-NOT complex, Cnot7, is also a metastasis modifying gene. We demonstrate that higher expression of Cnot7 drives tumor cell autonomous metastatic potential, which requires its deadenylase activity. Furthermore, metastasis promotion by CNOT7 is dependent on interaction with CNOT1 and TOB1. CNOT7 ribonucleoprotein-immunoprecipitation (RIP) and integrated transcriptome wide analyses reveal that CNOT7-regulated transcripts are enriched for a tripartite 3'UTR motif bound by RNA-binding proteins known to complex with CNOT7, TOB1, and CNOT1. Collectively, our data support a model of CNOT7, TOB1, CNOT1, and RNA-binding proteins collectively exerting post-transcriptional control on a metastasis suppressive transcriptional program to drive tumor cell metastasis.

Indexed as

AnimalsBreast NeoplasmsExoribonucleasesFemaleGene Expression RegulationGene Expression Regulation, NeoplasticHumansMammary Neoplasms, AnimalMiceNeoplasm MetastasisReceptors, CCR4Repressor ProteinsRNA StabilityTranscription FactorsTranscriptomeCCR4 protein, humanCNOT1 protein, humanCNOT7 protein, humanExoribonucleasesReceptors, CCR4Repressor ProteinsTranscription Factors

Identifiers

PMID26807845
PMCPMC4726497
OpenAlexW2265308074

What OpenQuestion holds

Textmetadata
LicenceCC0
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.