Evidence map›Paper›PMID 32518284›Full record

ArticleScientific reports2020

EXOSC9 depletion attenuates P-body formation, stress resistance, and tumorigenicity of cancer cells.

Seiko Yoshino, Yusuke Matsui, Yuya Fukui, Masahide Seki, Kiyoshi Yamaguchi, Akane Kanamori, Yurika Saitoh, Teppei Shimamura, Yutaka Suzuki, Yoichi Furukawa and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 31 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

15 authors at 4 institutions in 1 country.

Seiko Yoshino *Division of Molecular Pathology, the Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.
Yusuke Matsui *Biomedical and Health Informatics Unit, Department of Integrated Health Science, Nagoya University Graduate School of Medicine, Daiko-Minami, Higashi-ku, Nagoya, Aichi, Japan.
Yuya FukuiDivision of Cellular and Molecular Biology, the Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.
Masahide SekiDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, the University of Tokyo, Chiba, Japan.
Kiyoshi YamaguchiDivision of Clinical Genome Research, the Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.
Akane KanamoriDivision of Cellular and Molecular Biology, the Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.
Yurika SaitohDivision of Cellular and Molecular Biology, the Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.
Teppei ShimamuraDivision of Systems Biology, Nagoya University Graduate School of Medicine, Tsurumai-cho, Nagoya, Japan.
Yutaka SuzukiDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, the University of Tokyo, Chiba, Japan.
Yoichi FurukawaDivision of Clinical Genome Research, the Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.
Shuichi KanekoDepartment of System Biology, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Takaramachi, Kanazawa, Ishikawa, Japan.
Motoharu SeikiDivision of Cancer Cell Research, the Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.
Yoshinori MurakamiDivision of Molecular Pathology, the Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.
Jun-Ichiro InoueDivision of Cellular and Molecular Biology, the Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.
Takeharu SakamotoDepartment of System Biology, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Takaramachi, Kanazawa, Ishikawa, Japan. t-saka@staff.kanazawa-u.ac.jp.
The University of Tokyo · JPKanazawa University · JPNagoya University · JPTeikyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells adapt to various stress conditions by optimizing gene expression profiles via transcriptional and translational regulation. However, whether and how EXOSC9, a component of the RNA exosome complex, regulates adaptation to stress conditions and tumorigenicity in cancer cells remain unclear. Here, we examined the effects of EXOSC9 depletion on cancer cell growth under various stress conditions. EXOSC9 depletion attenuated growth and survival under various stress conditions in cancer cells. Interestingly, this also decreased the number of P-bodies, which are messenger ribonucleoprotein particles (mRNPs) required for stress adaptation. Meanwhile, EXOSC2/EXOSC4 depletion also attenuated P-body formation and stress resistance with decreased EXOSC9 protein. EXOSC9-mediated stress resistance and P-body formation were found to depend on the intact RNA-binding motif of this protein. Further, RNA-seq analyses identified 343 EXOSC9-target genes, among which, APOBEC3G contributed to defects in stress resistance and P-body formation in MDA-MB-231 cells. Finally, EXOSC9 also promoted xenografted tumor growth of MDA-MB-231 cells in an intact RNA-binding motif-dependent manner. Database analyses further showed that higher EXOSC9 activity, estimated based on the expression of 343 target genes, was correlated with poorer prognosis in some cancer patients. Thus, drugs targeting activity of the RNA exosome complex or EXOSC9 might be useful for cancer treatment.

Indexed as

AnimalsAPOBEC-3G DeaminaseBinding SitesCell Line, TumorCytoplasmic StructuresDNA DamageEndoplasmic Reticulum StressExosome Multienzyme Ribonuclease ComplexExosomesFemaleHumansMice, Inbred BALB COxidative StressRNA-Binding ProteinsStress, PhysiologicalXenograft Model Antitumor AssaysAPOBEC-3G DeaminaseAPOBEC3G protein, humanEXOSC9 protein, humanExosome Multienzyme Ribonuclease ComplexRNA-Binding Proteins

Identifiers

PMID32518284
PMCPMC7283315
OpenAlexW3034054640

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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.