Evidence map›Paper›PMID 37545364›Full record

ArticleThe EMBO journal2023

ADPGK-AS1 long noncoding RNA switches macrophage metabolic and phenotypic state to promote lung cancer growth.

Annika Karger, Siavash Mansouri, Matthias S Leisegang, Andreas Weigert, Stefan Günther, Carsten Kuenne, Ilka Wittig, Sven Zukunft, Stephan Klatt, Blerina Aliraj and 12 more

Abstract read
In one paragraph

Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

27 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Imaging immunometabolismImmunometabolism (Cobham, Surrey) · 2024
    Article
  19. Review
  20. mJournal of translational medicine · 2024
    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

22 authors.

Annika KargerMax 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, Germany.
Siavash MansouriMax 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, Germany.ORCID 0000-0003-0493-5084
Matthias S LeisegangInstitute for Cardiovascular Physiology, Medical Faculty, Goethe University Frankfurt, Frankfurt, Germany.ORCID 0000-0002-6084-6484
Andreas WeigertInstitute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, Frankfurt, Germany.ORCID 0000-0002-7529-1952
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, Germany.ORCID 0000-0002-5594-4549
Carsten 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, Germany.ORCID 0000-0001-8013-5906
Ilka WittigFunctional Proteomics, Medical School, Goethe University Frankfurt, Frankfurt, Germany.ORCID 0000-0002-9751-8054
Sven ZukunftInstitute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt, Germany.ORCID 0000-0002-1811-4562
Stephan KlattInstitute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt, Germany.
Blerina AlirajInstitute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, Frankfurt, Germany.
Laura V KlotzTranslational Lung Research Center (TLRC), Member of the DZL, Heidelberg, Germany.
Hauke WinterTranslational Lung Research Center (TLRC), Member of the DZL, Heidelberg, Germany.
Poornima MahavadiDepartment of Internal Medicine, Member of the DZL, Member of CPI, Justus Liebig University, Giessen, Germany.ORCID 0000-0002-7580-4738
Ingrid FlemingInstitute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt, Germany.ORCID 0000-0003-1881-3635
Clemens RuppertDepartment of Internal Medicine, Member of the DZL, Member of CPI, Justus Liebig University, Giessen, Germany.ORCID 0000-0002-0938-2469
Biruta WitteDepartment of General and Thoracic Surgery, University Hospital Giessen, Giessen, Germany.
Ibrahim AlkoudmaniDepartment of General and Thoracic Surgery, University Hospital Giessen, Giessen, Germany.
Stefan GattenlöhnerDepartment of Pathology, Justus Liebig University, Giessen, Germany.
Friedrich GrimmingerInstitute for Lung Health (ILH), Justus Liebig University, Giessen, Germany.
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, Germany.ORCID 0000-0003-1946-0894
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, Germany.ORCID 0000-0003-0440-8831
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, Germany.ORCID 0000-0003-1538-2091

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) influence the transcription of gene networks in many cell types, but their role in tumor-associated macrophages (TAMs) is still largely unknown. We found that the lncRNA ADPGK-AS1 was substantially upregulated in artificially induced M2-like human macrophages, macrophages exposed to lung cancer cells in vitro, and TAMs from human lung cancer tissue. ADPGK-AS1 is partly located within mitochondria and binds to the mitochondrial ribosomal protein MRPL35. Overexpression of ADPGK-AS1 in macrophages upregulates the tricarboxylic acid cycle and promotes mitochondrial fission, suggesting a phenotypic switch toward an M2-like, tumor-promoting cytokine release profile. Macrophage-specific knockdown of ADPGK-AS1 induces a metabolic and phenotypic switch (as judged by cytokine profile and production of reactive oxygen species) to a pro-inflammatory tumor-suppressive M1-like state, inhibiting lung tumor growth in vitro in tumor cell-macrophage cocultures, ex vivo in human tumor precision-cut lung slices, and in vivo in mice. Silencing ADPGK-AS1 in TAMs may thus offer a novel therapeutic strategy for lung cancer.

Indexed as

Lung NeoplasmsMicroRNAsRNA, Long NoncodingAnimalsCell Line, TumorCell MovementCell ProliferationCytokinesGene Expression Regulation, NeoplasticHumansMacrophagesMiceMitochondrial ProteinsRibosomal ProteinsCytokinesMicroRNAsMitochondrial ProteinsMRPL35 protein, humanRibosomal ProteinsRNA, Long NoncodingLong noncoding RNAsLung cancerMetabolic remodelingTumor-associated macrophagesTumor microenvironment

Identifiers

PMID37545364
PMCPMC10505917

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.