Evidence map›Paper›PMID 33077599›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

MNK2 governs the macrophage antiinflammatory phenotype.

Margarita Bartish, Dongmei Tong, Yangxun Pan, Majken Wallerius, Hui Liu, Johannes Ristau, Sabrina de Souza Ferreira, Tatjana Wallmann, Vincent van Hoef, Laia Masvidal and 15 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  16. Review
  17. Review
  18. Polysome Fractionation for Transcriptome-Wide Studies of mRNA Translation.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  19. Anota2seq Analysis for Transcriptome-Wide Studies of mRNA Translation.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  20. Article
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

25 authors at 6 institutions in 4 countries.

Margarita BartishDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.
Dongmei TongDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.ORCID 0000-0002-3468-5293
Yangxun PanDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.ORCID 0000-0002-3887-5852
Majken WalleriusDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.
Hui LiuDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.
Johannes RistauDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.
Sabrina de Souza FerreiraDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.ORCID 0000-0002-1779-8528
Tatjana WallmannDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.
Vincent van HoefDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.
Laia MasvidalDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.
Thomas KerzelSan Raffaele Telethon Institute for Gene Therapy, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.ORCID 0000-0003-0763-5319
Anne-Laure JolyDepartment of Laboratory Medicine, Division of Translational Cancer Research, Lund University Cancer Centre, Lund University, 22381 Lund, Sweden.ORCID 0000-0002-9686-5281
Christophe GoncalvesDepartment of Oncology, Segal Cancer Centre, Lady Davis Institute for Medical Research, Jewish General Hospital, McGill University, H3T 1E2 Montréal, QC, Canada.
Samuel E J PrestonDepartment of Experimental Medicine, Segal Cancer Centre, Lady Davis Institute for Medical Research, Jewish General Hospital, McGill University, H3T 1E2 Montréal, QC, Canada.ORCID 0000-0002-2618-8326
Talin EbrahimianDepartment of Experimental Medicine, Segal Cancer Centre, Lady Davis Institute for Medical Research, Jewish General Hospital, McGill University, H3T 1E2 Montréal, QC, Canada.
Christina SeitzDepartment of Laboratory Medicine, Division of Translational Cancer Research, Lund University Cancer Centre, Lund University, 22381 Lund, Sweden.
Jonas BerghDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden.
Kristian PietrasVita-Salute San Raffaele University, 20132 Milan, Italy.ORCID 0000-0001-6738-4705
Stephanie LehouxDepartment of Experimental Medicine, Segal Cancer Centre, Lady Davis Institute for Medical Research, Jewish General Hospital, McGill University, H3T 1E2 Montréal, QC, Canada.
Luigi NaldiniSan Raffaele Telethon Institute for Gene Therapy, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.
John AnderssonDepartment of Laboratory Medicine, Division of Translational Cancer Research, Lund University Cancer Centre, Lund University, 22381 Lund, Sweden.ORCID 0000-0003-2799-6349
Mario Leonardo SquadritoSan Raffaele Telethon Institute for Gene Therapy, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.ORCID 0000-0002-1188-0299
Sonia V Del RincónDepartment of Oncology, Segal Cancer Centre, Lady Davis Institute for Medical Research, Jewish General Hospital, McGill University, H3T 1E2 Montréal, QC, Canada.
Ola LarssonDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden; Ola.Larsson@ki.se Charlotte.Rolny@ki.se.ORCID 0000-0003-1412-1308
Charlotte RolnyDepartment of Oncology-Pathology, Karolinska Institutet, 17165 Solna, Sweden; Ola.Larsson@ki.se Charlotte.Rolny@ki.se.
Science for Life Laboratory · SEJewish General Hospital · CAVita-Salute San Raffaele University · ITLund University · SEKarolinska Institutet · SESun Yat-sen University · CN

Funding

CIHR PJT-162260
6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) continuously fine tune their immune modulatory properties, but how gene expression programs coordinate this immune cell plasticity is largely unknown. Selective mRNA translation, controlled by MNK1/MNK2 and mTOR pathways impinging on eIF4E, facilitates reshaping of proteomes without changes in abundance of corresponding mRNAs. Using polysome profiling developed for small samples we show that, during tumor growth, gene expression in TAMs is predominately modulated via mRNA-selective changes in translational efficiencies. These alterations in gene expression paralleled accumulation of antiinflammatory macrophages with augmented phosphorylation of eIF4E, a target of the MNK1 and MNK2 kinases, known to selectively modulate mRNA translation. Furthermore, suppression of the MNK2, but not the mTOR signaling pathway, reprogrammed antiinflammatory macrophages toward a proinflammatory phenotype with the ability to activate CD8

Indexed as

AnimalsCoculture TechniquesDisease Models, AnimalEukaryotic Initiation Factor-4EFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMacrophagesMCF-7 CellsMiceMice, TransgenicNaphthyridinesNeoplasmsPhosphorylationPrimary Cell Culture1-(4-(4-propionylpiperazin-1-yl)-3-(trifluoromethyl)phenyl)-9-(quinolin-3-yl)benzo(h)(1,6)naphthyridin-2(1H)-oneeIF4E protein, mouseEukaryotic Initiation Factor-4EMknk2 protein, mousemTOR protein, mouseNaphthyridinesProtein Serine-Threonine KinasesTOR Serine-Threonine KinaseseIF4EMNK2mRNA translationT cell activationtumor-associated macrophages

Identifiers

PMID33077599
PMCPMC7959504
OpenAlexW3092876137

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.