Evidence map›Paper›PMID 32203421›Full record

ArticleNature cell biology2020

Epigenetic remodelling shapes inflammatory renal cancer and neutrophil-dependent metastasis.

Jun Nishida, Yusaku Momoi, Kosuke Miyakuni, Yusuke Tamura, Kei Takahashi, Daizo Koinuma, Kohei Miyazono, Shogo Ehata

Abstract read
PubMed Publisher
In one paragraph

Article in Nature cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
8.7field-weighted citation impact, top 1% 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

97 citing papers in PubMed, 138 citations in OpenAlex.

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37 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Jun NishidaDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-5098-9361
Yusaku MomoiDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kosuke MiyakuniDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yusuke TamuraDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kei TakahashiDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Daizo KoinumaDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kohei MiyazonoDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. miyazono@m.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0001-7341-0172
Shogo EhataDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ehata-jun@umin.ac.jp.ORCID http://orcid.org/0000-0002-6740-9391
The University of Tokyo · JPTokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced clear cell renal cell carcinoma (ccRCC) frequently causes systemic inflammation. Recent studies have shown that cancer cells reshape the immune landscape by secreting cytokines or chemokines. This phenotype, called cancer-cell-intrinsic inflammation, triggers a metastatic cascade. Here, we identified the functional role and regulatory mechanism of inflammation driven by advanced ccRCC cells. The inflammatory nature of advanced ccRCC was recapitulated in a preclinical model of ccRCC. Amplification of cancer-cell-intrinsic inflammation during ccRCC progression triggered neutrophil-dependent lung metastasis. Massive expression of inflammation-related genes was transcriptionally activated by epigenetic remodelling through mechanisms such as DNA demethylation and super-enhancer formation. A bromodomain and extra-terminal motif inhibitor synchronously suppressed C-X-C-type chemokines in ccRCC cells and decreased neutrophil-dependent lung metastasis. Overall, our findings provide insight into the nature of inflammatory ccRCC, which triggers metastatic cascades, and suggest a potential therapeutic strategy.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticAnimalsCarcinoma, Renal CellCell Line, TumorChemokines, CXCDisease ProgressionGene Expression ProfilingHumansInflammationKidney NeoplasmsLung NeoplasmsLymphatic MetastasisMaleMiceMice, NudeChemokines, CXCNeoplasm Proteins

Identifiers

PMID32203421
OpenAlexW3012839625

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.