Evidence map›Paper›PMID 35501580›Full record

ArticleCellular and molecular life sciences : CMLS2022

RIP140 inhibits glycolysis-dependent proliferation of breast cancer cells by regulating GLUT3 expression through transcriptional crosstalk between hypoxia induced factor and p53.

Valentin Jacquier, Delphine Gitenay, Samuel Fritsch, Sandrine Bonnet, Balázs Győrffy, Stéphan Jalaguier, Laetitia K Linares, Vincent Cavaillès, Catherine Teyssier

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  12. Importance of GLUT Transporters in Disease Diagnosis and Treatment.International journal of molecular sciences · 2022
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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 3 institutions in 2 countries.

Valentin JacquierIRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM U1194, University of Montpellier, ICM, 34298, Montpellier, France.
Delphine GitenayIRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM U1194, University of Montpellier, ICM, 34298, Montpellier, France.
Samuel FritschIRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM U1194, University of Montpellier, ICM, 34298, Montpellier, France.
Sandrine BonnetIRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM U1194, University of Montpellier, ICM, 34298, Montpellier, France.
Balázs GyőrffyDepartment of Bioinformatics, Semmelweis University and TTK Lendület Cancer Biomarker Research Group, Budapest, Hungary.
Stéphan JalaguierIRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM U1194, University of Montpellier, ICM, 34298, Montpellier, France.
Laetitia K LinaresIRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM U1194, University of Montpellier, ICM, 34298, Montpellier, France.
Vincent Cavaillès *IRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM U1194, University of Montpellier, ICM, 34298, Montpellier, France. vincent.cavailles@inserm.fr.
Catherine Teyssier *IRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM U1194, University of Montpellier, ICM, 34298, Montpellier, France. catherine.teyssier@inserm.fr.ORCID http://orcid.org/0000-0003-4937-6503
Inserm · FRCentre National de la Recherche Scientifique · FRSemmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycolysis is essential to support cancer cell proliferation, even in the presence of oxygen. The transcriptional co-regulator RIP140 represses the activity of transcription factors that drive cell proliferation and metabolism and plays a role in mammary tumorigenesis. Here we use cell proliferation and metabolic assays to demonstrate that RIP140-deficiency causes a glycolysis-dependent increase in breast tumor growth. We further demonstrate that RIP140 reduces the transcription of the glucose transporter GLUT3 gene, by inhibiting the transcriptional activity of hypoxia inducible factor HIF-2α in cooperation with p53. Interestingly, RIP140 expression was significantly associated with good prognosis only for breast cancer patients with tumors expressing low GLUT3, low HIF-2α and high p53, thus confirming the mechanism of RIP140 anti-tumor activity provided by our experimental data. Overall, our work establishes RIP140 as a critical modulator of the p53/HIF cross-talk to inhibit breast cancer cell glycolysis and proliferation.

Indexed as

Breast NeoplasmsTumor Suppressor Protein p53Basic Helix-Loop-Helix ProteinsCell ProliferationFemaleGlucose Transporter Type 3GlycolysisHumansHypoxiaNuclear Receptor Interacting Protein 1Basic Helix-Loop-Helix ProteinsGlucose Transporter Type 3NRIP1 protein, humanNuclear Receptor Interacting Protein 1SLC2A3 protein, humanTumor Suppressor Protein p53Breast cancerCancer cell metabolismGLUT3GlycolysisHIFp53RIP140Transcription factors

Identifiers

PMID35501580
PMCPMC9061696
OpenAlexW4225380092

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.