Evidence map›Paper›PMID 33290632›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2021

G-quadruplex-forming nucleic acids interact with splicing factor 3B subunit 2 and suppress innate immune gene expression.

Kyoko Matsumoto, Keiji Okamoto, Sachiko Okabe, Risa Fujii, Koji Ueda, Kenichi Ohashi, Hiroyuki Seimiya

Open access · hybridAbstract read
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

12 citing papers in PubMed, 12 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Kyoko MatsumotoDivision of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Keiji OkamotoDivision of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Sachiko OkabeDivision of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Risa FujiiCancer Proteomics Group, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Koji UedaCancer Proteomics Group, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
Kenichi OhashiDepartment of Pathology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.
Hiroyuki SeimiyaDivision of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID https://orcid.org/0000-0003-3314-9736
Japanese Foundation For Cancer Research · JPTokyo Medical and Dental University · JP

Funding

Japan Agency for Medical Research and DevelopmentJapan Society for the Promotion of Science 18K07252Japan Society for the Promotion of Science 20H04789Japan Society for the Promotion of Science 20K21555Nippon Foundation
6 · The paper itself

Abstract

G-quadruplex (G4), a non-canonical higher-order structure formed by guanine-rich nucleic acid sequences, affects various genetic events in cis, including replication, transcription and translation. Whereas up-regulation of innate immune/interferon-stimulated genes (ISGs) is implicated in cancer progression, G4-forming oligonucleotides that mimic telomeric repeat-containing RNA suppress ISG induction in three-dimensional (3D) culture of cancer cells. However, it is unclear how G4 suppresses ISG expression in trans. In this study, we found that G4 binding to splicing factor 3B subunit 2 (SF3B2) down-regulated STAT1 phosphorylation and ISG expression in 3D-cultured cancer cells. Liquid chromatography-tandem mass spectrometry analysis identified SF3B2 as a G4-binding protein. Either G4-forming oligonucleotides or SF3B2 knockdown suppressed ISG induction, whereas Phen-DC3, a G4-stabilizing compound, reversed the inhibitory effect of G4-forming oligonucleotides on ISG induction. Phen-DC3 inhibited SF3B2 binding to G4 in vitro. SF3B2-mediated ISG induction appeared to occur independently of RNA splicing because SF3B2 knockdown did not affect pre-mRNA splicing under the experimental conditions, and pharmacological inhibition of splicing by pladienolide B did not repress ISG induction. These observations suggest that G4 disrupts the ability of SF3B2 to induce ISGs in cancer. We propose a new mode for gene regulation, which employs G4 as an inhibitory trans-element.

Indexed as

Gene Expression RegulationG-QuadruplexesCell Line, TumorCytokinesFused-Ring CompoundsGene Knockdown TechniquesGene OntologyHumansImmunity, InnateLigandsModels, BiologicalNucleic AcidsOligonucleotidesProtein BindingRNA SplicingRNA Splicing FactorsCytokinesFused-Ring CompoundsISG15 protein, humanLigandsNucleic AcidsOligonucleotidesPhenDC3RNA Splicing FactorsSF3B2 protein, humanSTAT1 Transcription FactorUbiquitinscancerG-quadruplexinnate immune geneinterferon-stimulated geneSF3B2splicing factortelomere

Identifiers

PMID33290632
PMCPMC7898707
OpenAlexW3111789495

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.