Evidence map›Paper›PMID 32246865›Full record

ArticleCancer science2020

Ribosomal protein S6 promotes stem-like characters in glioma cells.

Yuki Shirakawa, Takuichiro Hide, Michiko Yamaoka, Yuki Ito, Naofumi Ito, Kunimasa Ohta, Naoki Shinojima, Akitake Mukasa, Hideyuki Saito, Hirofumi Jono

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

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  14. Review
  15. Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021
    Review
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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

10 authors at 3 institutions in 1 country.

Yuki ShirakawaDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-6775-0952
Takuichiro HideDepartment of Neurosurgery, Kitasato University School of Medicine, Sagamihara, Japan.
Michiko YamaokaDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
Yuki ItoDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
Naofumi ItoDepartment of Developmental Neurobiology, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.
Kunimasa OhtaDepartment of Developmental Neurobiology, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.
Naoki ShinojimaDepartment of Neurosurgery, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Akitake MukasaDepartment of Neurosurgery, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Hideyuki SaitoDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
Hirofumi JonoDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
Kumamoto University · JPKumamoto City Hospital · JPKitasato University · JP

Funding

Japan Society for the Promotion of Science 18H02591Japan Society for the Promotion of Science 26713006
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM), a lethal brain tumor developing in the white matter of the adult brain, contains a small population of GBM stem cells (GSCs), which potentially cause chemotherapeutic resistance and tumor recurrence. However, the mechanisms underlying the pathogenesis and maintenance of GSCs remain largely unknown. A recent study reported that incorporation of ribosomes and ribosomal proteins into somatic cells promoted lineage trans-differentiation toward multipotency. This study aimed to investigate the mechanism underlying stemness acquisition in GBM cells by focusing on 40S ribosomal protein S6 (RPS6). RPS6 was significantly upregulated in high-grade glioma and localized at perivascular, perinecrotic, and border niches in GBM tissues. siRNA-mediated RPS6 knock-down significantly suppressed the characteristics of GSCs, including their tumorsphere potential and GSC marker expression; STAT3 was downregulated in GBM cells. RPS6 overexpression enhanced the tumorsphere potential of GSCs and these effects were attenuated by STAT3 inhibitor (AG490). Moreover, RPS6 expression was significantly correlated with SOX2 expression in different glioma grades. Immunohistochemistry data herein indicated that RPS6 was predominant in GSC niches, concurrent with the data from IVY GAP databases. Furthermore, RPS6 and other ribosomal proteins were upregulated in GSC-predominant areas in this database. The present results indicate that, in GSC niches, ribosomal proteins play crucial roles in the development and maintenance of GSCs and are clinically associated with chemoradioresistance and GBM recurrence.

Indexed as

AdultAgedBrain NeoplasmsChildFemaleGlioblastomaHumansInfantMaleMiddle AgedNeoplastic Stem CellsRibosomal Protein S6Ribosomal Protein S6cancer stem cellGBM stem-like cellsglioblastomaribosomal protein S6ribosome

Identifiers

PMID32246865
PMCPMC7293102
OpenAlexW3014959179

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.