Evidence map›Paper›PMID 37845228›Full record

ArticleNature communications2023

Sleeping Beauty transposon mutagenesis identified genes and pathways involved in inflammation-associated colon tumor development.

Kana Shimomura, Naoko Hattori, Naoko Iida, Yukari Muranaka, Kotomi Sato, Yuichi Shiraishi, Yasuhito Arai, Natsuko Hama, Tatsuhiro Shibata, Daichi Narushima and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. PRDM Proteins Orchestrate Colorectal Cancer Tumorigenesis.International journal of molecular sciences · 2026
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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

14 authors at 4 institutions in 2 countries.

Kana ShimomuraThe Laboratory of Molecular Genetics, National Cancer Center Research Institute, Tokyo, Japan.
Naoko HattoriDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Naoko IidaDivision of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo, Japan.
Yukari MuranakaThe Laboratory of Molecular Genetics, National Cancer Center Research Institute, Tokyo, Japan.
Kotomi SatoThe Laboratory of Molecular Genetics, National Cancer Center Research Institute, Tokyo, Japan.
Yuichi ShiraishiDivision of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo, Japan.ORCID http://orcid.org/0000-0001-6144-5845
Yasuhito AraiDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.ORCID http://orcid.org/0000-0001-6306-9409
Natsuko HamaDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Tatsuhiro ShibataDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Daichi NarushimaDivision of Bioinformatics, National Cancer Center Research Institute, Tokyo, Japan.ORCID http://orcid.org/0000-0003-4639-4052
Mamoru KatoDivision of Bioinformatics, National Cancer Center Research Institute, Tokyo, Japan.ORCID http://orcid.org/0000-0002-8485-8316
Hiroyuki TakamaruEndoscopy Division, National Cancer Center Hospital, Tokyo, Japan.
Koji OkamotoAdvanced Comprehensive Research Organization, Teikyo University, Tokyo, Japan.
Haruna TakedaThe Laboratory of Molecular Genetics, National Cancer Center Research Institute, Tokyo, Japan. hartaked@ncc.go.jp.ORCID http://orcid.org/0000-0002-1643-2524
Hoshi University · JPNational Cancer Center Hospital East · JPNational Cancer Research Institute · GBTeikyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation promotes development and progression of colorectal cancer (CRC). To comprehensively understand the molecular mechanisms underlying the development and progression of inflamed CRC, we perform in vivo screening and identify 142 genes that are frequently mutated in inflammation-associated colon tumors. These genes include senescence and TGFβ-activin signaling genes. We find that TNFα can induce stemness and activate senescence signaling by enhancing cell plasticity in colonic epithelial cells, which could act as a selective pressure to mutate senescence-related genes in inflammation-associated colonic tumors. Furthermore, we show the efficacy of the Cdk4/6 inhibitor in vivo for inflammation-associated colonic tumors. Finally, we functionally validate that Arhgap5 and Mecom are tumor suppressor genes, providing possible therapeutic targets for CRC. Thus, we demonstrate the importance of the inactivation of senescence pathways in CRC development and progression in an inflammatory microenvironment, which can help progress toward precision medicine.

Indexed as

Colonic NeoplasmsColorectal NeoplasmsHumansInflammationMutagenesisSignal TransductionTumor Microenvironment

Identifiers

PMID37845228
PMCPMC10579371
OpenAlexW4387692758

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.