Evidence map›Paper›PMID 34046694›Full record

ArticleCellular and molecular life sciences : CMLS2021

Dual regulation of fatty acid synthase (FASN) expression by O-GlcNAc transferase (OGT) and mTOR pathway in proliferating liver cancer cells.

Sadia Raab, Alexis Gadault, Ninon Very, Amélie Decourcelle, Steffi Baldini, Céline Schulz, Marlène Mortuaire, Quentin Lemaire, Stéphan Hardivillé, Vanessa Dehennaut and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

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  6. Mammalian fatty acid synthase andBiochemistry and biophysics reports · 2026
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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 1 institution in 1 country.

Sadia RaabUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.ORCID http://orcid.org/0000-0003-4492-9340
Alexis GadaultInstitut Necker-Enfants Malades (INEM), INSERM U1151/CNRS UMR 8253, Université de Paris , 75014, Paris, France.ORCID http://orcid.org/0000-0001-5188-1328
Ninon VeryUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.ORCID http://orcid.org/0000-0003-4250-5819
Amélie DecourcelleUniversité de Lille, CNRS, Inserm, CHU Lille, UMR9020-U1277-CANTHER-Cancer Heterogeneity, Plasticity and Resistance to Therapies, 59000, Lille, France.
Steffi BaldiniUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.ORCID http://orcid.org/0000-0002-8673-0770
Céline SchulzUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.ORCID http://orcid.org/0000-0003-3867-1443
Marlène MortuaireUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.
Quentin LemaireUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.ORCID http://orcid.org/0000-0002-1403-678X
Stéphan HardivilléUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.ORCID http://orcid.org/0000-0002-3554-277X
Vanessa DehennautUniversité de Lille, CNRS, Inserm, CHU Lille, UMR9020-U1277-CANTHER-Cancer Heterogeneity, Plasticity and Resistance to Therapies, 59000, Lille, France.ORCID http://orcid.org/0000-0001-6421-0793
Ikram El Yazidi-BelkouraUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.ORCID http://orcid.org/0000-0002-5323-7509
Anne-Sophie Vercoutter-EdouartUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.ORCID http://orcid.org/0000-0002-3243-7122
Ganna PanasyukInstitut Necker-Enfants Malades (INEM), INSERM U1151/CNRS UMR 8253, Université de Paris , 75014, Paris, France.ORCID http://orcid.org/0000-0002-5591-848X
Tony LefebvreUniversité de Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France. tony.lefebvre@univ-lille.fr.ORCID http://orcid.org/0000-0001-9883-2240
Centre National de la Recherche Scientifique · FR

Funding

Agence Nationale de la Recherche ANR-JCJC-NUTRISENSPIK-16-CE14-0029
6 · The paper itself

Abstract

Fatty acid synthase (FASN) participates in many fundamental biological processes, including energy storage and signal transduction, and is overexpressed in many cancer cells. We previously showed in a context of lipogenesis that FASN is protected from degradation by its interaction with O-GlcNAc transferase (OGT) in a nutrient-dependent manner. We and others also reported that OGT and O-GlcNAcylation up-regulate the PI3K/AKT/mTOR pathway that senses mitogenic signals and nutrient availability to drive cell cycle. Using biochemical and microscopy approaches, we show here that FASN co-localizes with OGT in the cytoplasm and, to a lesser extent, in the membrane fraction. This interaction occurs in a cell cycle-dependent manner, following the pattern of FASN expression. Moreover, we show that FASN expression depends on OGT upon serum stimulation. The level of FASN also correlates with the activation of the PI3K/AKT/mTOR pathway in hepatic cell lines, and in livers of obese mice and in a chronically activated insulin and mTOR signaling mouse model (PTEN-null mice). These results indicate that FASN is under a dual control of O-GlcNAcylation and mTOR pathways. In turn, blocking FASN with the small-molecule inhibitor C75 reduces both OGT and O-GlcNAcylation levels, and mTOR activation, highlighting a novel reciprocal regulation between these actors. In addition to the role of O-GlcNAcylation in tumorigenesis, our findings shed new light on how aberrant activity of FASN and mTOR signaling may promote the emergence of hepatic tumors.

Indexed as

AnimalsApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell ProliferationFatty Acid Synthase, Type IGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMiceMice, Inbred C57BLMice, ObeseN-AcetylglucosaminyltransferasesTOR Serine-Threonine KinasesTumor Cells, CulturedBiomarkers, TumorFASN protein, humanFatty Acid Synthase, Type IMTOR protein, humanN-AcetylglucosaminyltransferasesOGT protein, humanTOR Serine-Threonine KinasesCell proliferationOb/ob miceProtein interactionsProximity ligation assaysiRNA

Identifiers

PMID34046694
PMCPMC11072354
OpenAlexW3164852094

What OpenQuestion holds

Textmetadata
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.