Evidence map›Paper›PMID 34426493›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Pericentromeric noncoding RNA changes DNA binding of CTCF and inflammatory gene expression in senescence and cancer.

Kenichi Miyata, Yoshinori Imai, Satoshi Hori, Mika Nishio, Tze Mun Loo, Ryo Okada, Liying Yang, Tomoyoshi Nakadai, Reo Maruyama, Risa Fujii and 15 more

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

47 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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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

25 authors at 8 institutions in 1 country.

Kenichi MiyataProject for Cellular Senescence, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.ORCID 0000-0002-8618-3105
Yoshinori ImaiProject for Cellular Senescence, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Satoshi HoriProject for Cellular Senescence, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Mika NishioProject for Cellular Senescence, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Tze Mun LooProject for Cellular Senescence, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.ORCID 0000-0001-5725-1423
Ryo OkadaProject for Cellular Senescence, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Liying YangProject for Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Tomoyoshi NakadaiProject for Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Reo MaruyamaProject for Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Risa FujiiProject for Personalized Cancer Medicine, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Koji UedaProject for Personalized Cancer Medicine, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Li JiangDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 466-8550 Nagoya, Japan.
Hao ZhengDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 466-8550 Nagoya, Japan.
Shinya ToyokuniDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 466-8550 Nagoya, Japan.ORCID 0000-0002-5757-1109
Toyonori SakataLaboratory of Genome Structure and Function, Institute for Quantitative Biosciences, The University of Tokyo, 113-0032 Tokyo, Japan.
Katsuhiko ShirahigeLaboratory of Genome Structure and Function, Institute for Quantitative Biosciences, The University of Tokyo, 113-0032 Tokyo, Japan.
Ryosuke KojimaGraduate School of Medicine, The University of Tokyo, 113-0033 Tokyo, Japan.ORCID 0000-0002-3792-9222
Mizuho NakayamaDivision of Genetics, Cancer Research Institute, Kanazawa University, 920-1192 Kanazawa, Japan.ORCID 0000-0002-0464-3519
Masanobu OshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, 920-1192 Kanazawa, Japan.ORCID 0000-0002-3304-0004
Satoshi NagayamaGastroenterological Center, Department of Gastroenterological Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.ORCID 0000-0001-9632-914X
Hiroyuki SeimiyaDivision of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.ORCID 0000-0003-3314-9736
Toru HirotaExperimental Pathology, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan.
Hideyuki SayaDivision of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, 160-8582 Tokyo, Japan.
Eiji HaraDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, 565-0871 Osaka, Japan.ORCID 0000-0001-7821-3960
Akiko TakahashiProject for Cellular Senescence, Cancer Institute, Japanese Foundation for Cancer Research, 135-8550 Tokyo, Japan; akiko.takahashi@jfcr.or.jp.ORCID 0000-0003-1904-7645
Japanese Foundation For Cancer Research · JPNagoya University · JPKanazawa University · JPThe University of Tokyo · JPJapan Agency for Medical Research and Development · JPJapan Science and Technology Agency · JPKeio University · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence causes a dramatic alteration of chromatin organization and changes the gene expression profile of proinflammatory factors, thereby contributing to various age-related pathologies through the senescence-associated secretory phenotype (SASP). Chromatin organization and global gene expression are maintained by the CCCTC-binding factor (CTCF); however, the molecular mechanism underlying CTCF regulation and its association with SASP gene expression remains unclear. We discovered that noncoding RNA (ncRNA) derived from normally silenced pericentromeric repetitive sequences directly impairs the DNA binding of CTCF. This CTCF disturbance increases the accessibility of chromatin and activates the transcription of SASP-like inflammatory genes, promoting malignant transformation. Notably, pericentromeric ncRNA was transferred into surrounding cells via small extracellular vesicles acting as a tumorigenic SASP factor. Because CTCF blocks the expression of pericentromeric ncRNA in young cells, the down-regulation of CTCF during cellular senescence triggers the up-regulation of this ncRNA and SASP-related inflammatory gene expression. In this study, we show that pericentromeric ncRNA provokes chromosomal alteration by inhibiting CTCF, leading to a SASP-like inflammatory response in a cell-autonomous and non-cell-autonomous manner and thus may contribute to the risk of tumorigenesis during aging.

Indexed as

AgingAnimalsCellular SenescenceCentromereDNADNA-Binding ProteinsDNA, NeoplasmFemaleGene Expression RegulationHEK293 CellsHumansInflammationMiceMice, Inbred BALB CNeoplasmsProtein BindingCTCFL protein, humanDNADNA-Binding ProteinsDNA, NeoplasmRNA, UntranslatedCTCFpericentromeric RNAsenescencesenescence-associated secretory phenotypesmall extracellular vesicles

Identifiers

PMID34426493
PMCPMC8536346
OpenAlexW3195865705

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.