Evidence map›Paper›PMID 40436847›Full record

ArticleNature communications2025

RNF20 links the DNA damage response and metabolic rewiring in lung cancer through HIF1α.

Hao Liu, Yongqin Tang, Anshu Singh, Joaquim Vong, Julio Cordero, Arthur Mathes, Rui Gao, Yanhan Jia, Boyan K Garvalov, Till Acker and 11 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Decoding RNF20: an epigenetic modifier and beyond.Frontiers in cell and developmental biology · 2026
    Review
  9. Review
  10. Article
  11. Review
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

21 authors.

Hao Liu *Department of Cardiovascular Genomics and Epigenomics, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Yongqin Tang *Department of Cardiovascular Genomics and Epigenomics, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Anshu Singh *Department of Cardiovascular Genomics and Epigenomics, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Joaquim VongMax Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.ORCID http://orcid.org/0000-0002-5859-2008
Julio CorderoDepartment of Cardiovascular Genomics and Epigenomics, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Arthur MathesDepartment of Cardiovascular Genomics and Epigenomics, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Rui GaoDepartment of Cardiovascular Genomics and Epigenomics, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID http://orcid.org/0009-0006-1400-4637
Yanhan JiaDepartment of Cardiovascular Genomics and Epigenomics, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Boyan K GarvalovDepartment of Microvascular Biology and Pathobiology, European Center for Angioscience (ECAS) and Mannheim Institute for Innate Immunoscience (MI3), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID http://orcid.org/0000-0003-0013-9064
Till AckerInstitute of Neuropathology, Justus Liebig University, Giessen, Germany.ORCID http://orcid.org/0000-0001-6357-7227
Gernot PoschetCentre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-5344-0865
Rüdiger HellCentre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-6238-4818
Marc A SchneiderTranslational Lung Research Center (TLRC) Heidelberg, German Center for Lung Research (DZL), Heidelberg, Germany.ORCID http://orcid.org/0000-0001-8269-3821
Joerg HeinekeCardiovascular Physiology, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID http://orcid.org/0000-0002-1541-3030
Thomas WielandGerman Centre for Cardiovascular Research (DZHK), Mannheim, Germany.ORCID http://orcid.org/0000-0001-8262-8261
Guillermo BarretoUniversité de Lorraine, CNRS, Laboratoire IMoPA, UMR, 7365, Nancy, France.ORCID http://orcid.org/0000-0002-7777-4712
Adelheid CerwenkaImmunobiochemistry, Mannheim Institute for Innate Immunoscience (MI3) and European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID http://orcid.org/0000-0001-6977-3536
Michael PotenteMax Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.ORCID http://orcid.org/0000-0002-5689-0036
Sofia-Iris BibliInstitute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt am Main, Germany.
Rajkumar SavaiInstitute for Lung Health (ILH), Justus Liebig University, 35392, Giessen, Germany.ORCID http://orcid.org/0000-0003-1538-2091
Gergana DobrevaDepartment of Cardiovascular Genomics and Epigenomics, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Gergana.Dobreva@medma.uni-heidelberg.de.ORCID http://orcid.org/0000-0002-4814-9416

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) CRC 1366 (project A03)Deutsche Forschungsgemeinschaft (German Research Foundation) TRR81 (Project B07)
6 · The paper itself

Abstract

Defective DNA repair and metabolic rewiring are highly intertwined in promoting the development and progression of cancer. However, the molecular players at their interface remain poorly understood. Here we show that an RNF20-HIF1α axis links the DNA damage response and metabolic reprogramming in lung cancer. We demonstrate that RNF20, which catalyzes monoubiquitylation of histone H2B (H2Bub1), controls Rbx1 expression and thereby the activity of the VHL ubiquitin ligase complex and HIF1α levels. Ablation of a single Rnf20 allele significantly increases the incidence of lung tumors in mice. Mechanistically, Rnf20 haploinsufficiency results in inadequate tumor suppression via the Rnf20-H2Bub1-p53 axis and induces DNA damage, cell growth, epithelial-mesenchymal transition (EMT), and metabolic rewiring through HIF1α-mediated RNA polymerase II promoter-proximal pause release, which is independent of H2Bub1. Importantly, decreased RNF20 levels correlate with increased expression of HIF1α and its target genes, suggesting HIF1α inhibition as a promising therapeutic approach for lung cancer patients with reduced RNF20 activity.

Indexed as

DNA DamageHypoxia-Inducible Factor 1, alpha SubunitLung NeoplasmsUbiquitin-Protein LigasesAnimalsCell Line, TumorDNA RepairEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistonesHumansMaleMiceMice, KnockoutRNA Polymerase IIHIF1A protein, humanHif1a protein, mouseHistonesHypoxia-Inducible Factor 1, alpha SubunitRNA Polymerase IIRNF20 protein, humanRNF20 protein, mouseTumor Suppressor Protein p53Ubiquitin-Protein LigasesVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID40436847
PMCPMC12120090

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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.