Evidence map›Paper›PMID 32548260›Full record

ArticleScience advances2020

Reprogramming of tumor-associated macrophages by targeting β-catenin/FOSL2/ARID5A signaling: A potential treatment of lung cancer.

Poonam Sarode, Xiang Zheng, Georgia A Giotopoulou, Andreas Weigert, Carste Kuenne, Stefan Günther, Aleksandra Friedrich, Stefan Gattenlöhner, Thorsten Stiewe, Bernhard Brüne and 5 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

121 citing papers in PubMed, 1 synthesis or guideline pooled it, 176 citations in OpenAlex.

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  11. Macrophage β-catenin-Ihh axis induces hepatic stellate cell activation and fibrosis in metabolic dysfunction-associated steatohepatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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61 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 5 institutions in 1 country.

Poonam SarodeMax Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim 61231, Germany.ORCID 0000-0002-3004-1132
Xiang ZhengMax Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim 61231, Germany.ORCID 0000-0001-7588-825X
Georgia A GiotopoulouLaboratory for Molecular Respiratory Carcinogenesis, Department of Physiology, Faculty of Medicine, University of Patras, Rio, 26504, Greece and Lung Carcinogenesis Laboratory, Comprehensive Pneumology Center (CPC) and Institute for Lung Biology and Disease (iLBD), University Hospital, Ludwig-Maximilians University and Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich 81377, Germany.ORCID 0000-0001-5621-6802
Andreas WeigertInstitute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, Frankfurt 60323, Germany.ORCID 0000-0002-7529-1952
Carste KuenneMax Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim 61231, Germany.ORCID 0000-0001-8013-5906
Stefan GüntherMax Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim 61231, Germany.ORCID 0000-0002-5594-4549
Aleksandra FriedrichMax Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim 61231, Germany.
Stefan GattenlöhnerDepartment of Pathology, Member of the DZL, Justus Liebig University, Giessen 35390, Germany.ORCID 0000-0002-8673-6777
Thorsten StieweInstitute of Molecular Oncology, Philipps-University Marburg, Member of the DZL, Marburg 35043, Germany.ORCID 0000-0003-0134-7826
Bernhard BrüneInstitute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, Frankfurt 60323, Germany.ORCID 0000-0001-8237-2841
Friedrich GrimmingerDepartment of Internal Medicine, Member of the DZL, Member of CPI, Justus Liebig University, 35392 Giessen, Germany.ORCID 0000-0001-8725-6276
Georgios T StathopoulosLaboratory for Molecular Respiratory Carcinogenesis, Department of Physiology, Faculty of Medicine, University of Patras, Rio, 26504, Greece and Lung Carcinogenesis Laboratory, Comprehensive Pneumology Center (CPC) and Institute for Lung Biology and Disease (iLBD), University Hospital, Ludwig-Maximilians University and Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich 81377, Germany.ORCID 0000-0002-9215-6461
Soni Savai PullamsettiMax Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim 61231, Germany.ORCID 0000-0003-0440-8831
Werner SeegerMax Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim 61231, Germany.ORCID 0000-0003-1946-0894
Rajkumar SavaiMax Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), Bad Nauheim 61231, Germany.ORCID 0000-0003-1538-2091
Max Planck Institute for Heart and Lung Research · DEJustus-Liebig-Universität Gießen · DEGoethe University Frankfurt · DEGerman Center for Lung Research · DEPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) influence lung tumor development by inducing immunosuppression. Transcriptome analysis of TAMs isolated from human lung tumor tissues revealed an up-regulation of the Wnt/β-catenin pathway. These findings were reproduced in a newly developed in vitro "trained" TAM model. Pharmacological and macrophage-specific genetic ablation of β-catenin reprogrammed M2-like TAMs to M1-like TAMs both in vitro and in various in vivo models, which was linked with the suppression of primary and metastatic lung tumor growth. An in-depth analysis of the underlying signaling events revealed that β-catenin-mediated transcriptional activation of FOS-like antigen 2 (FOSL2) and repression of the AT-rich interaction domain 5A (ARID5A) drive gene regulatory switch from M1-like TAMs to M2-like TAMs. Moreover, we found that high expressions of β-catenin and FOSL2 correlated with poor prognosis in patients with lung cancer. In conclusion, β-catenin drives a transcriptional switch in the lung tumor microenvironment, thereby promoting tumor progression and metastasis.

Indexed as

beta CateninLung NeoplasmsCell Line, TumorFos-Related Antigen-2HumansTumor-Associated MacrophagesTumor MicroenvironmentWnt Signaling Pathwaybeta CateninFOSL2 protein, humanFos-Related Antigen-2

Identifiers

PMID32548260
PMCPMC7274802
OpenAlexW3033360413

What OpenQuestion holds

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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.