Evidence map›Paper›PMID 32885530›Full record

ArticleCancer science2020

RBPJ contributes to the malignancy of glioblastoma and induction of proneural-mesenchymal transition via IL-6-STAT3 pathway.

Guangtao Zhang, Shingo Tanaka, Shabierjiang Jiapaer, Hemragul Sabit, Sho Tamai, Masashi Kinoshita, Mitsutoshi Nakada

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

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  15. Roles of STAT3 in the pathogenesis and treatment of glioblastoma.Frontiers in cell and developmental biology · 2023
    Review
  16. Article
  17. Review
  18. Genomic Analysis of Abnormal DNAM Methylation in Parathyroid Tumors.International journal of endocrinology · 2022
    Article
  19. Article
  20. Article
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 1 institution in 2 countries.

Guangtao ZhangDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Shingo TanakaDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Shabierjiang JiapaerDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Hemragul SabitDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Sho TamaiDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Masashi KinoshitaDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Mitsutoshi NakadaDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.ORCID https://orcid.org/0000-0001-9419-6101
Kanazawa University · JP

Funding

China Scholarship CouncilJSPS KAKENHI 17K10858JSPS KAKENHI 18H02910Kobayashi International Scholarship Foundation
6 · The paper itself

Abstract

Notch signaling plays a pivotal role in many cancers, including glioblastoma (GBM). Recombination signal binding protein for immunoglobulin kappa J region (RBPJ) is a key transcription factor of the Notch signaling pathway. Here, we interrogated the function of RBPJ in GBM. Firstly, RBPJ expression of GBM samples was examined. Then, we knocked down RBPJ expression in 2 GBM cell lines (U251 and T98) and 4 glioblastoma (GBM) stem-like cell lines derived from surgical samples of GBM (KGS01, KGS07, KGS10 and KGS15) to investigate the effect on cell proliferation, invasion, stemness, and tumor formation ability. Expression of possible downstream targets of RBPJ was also assessed. RBPJ was overexpressed in the GBM samples, downregulation of RBPJ reduced cell proliferation and the invasion ability of U251 and T98 cells and cell proliferation ability and stemness of glioblastoma stem-like cells (GSC) lines. These were accompanied by reduced IL-6 expression, reduced activation of STAT3, and inhibited proneural-mesenchymal transition (PMT). Tumor formation and PMT were also impaired by RBPJ knockdown in vivo. In conclusion, RBPJ promotes cell proliferation, invasion, stemness, and tumor initiation ability in GBM cells through enhanced activation of IL-6-STAT3 pathway and PMT, inhibition of RBPJ may constitute a prospective treatment for GBM.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionBrain NeoplasmsCell Line, TumorCell ProliferationGene Knockdown TechniquesGlioblastomaHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinImmunohistochemistryInterleukin-6Neoplasm GradingNeoplasm StagingNeoplastic Stem CellsSTAT3 Transcription FactorImmunoglobulin J Recombination Signal Sequence-Binding ProteinInterleukin-6RBPJ protein, humanSTAT3 protein, humanSTAT3 Transcription Factorglioblastomaglioblastoma stem-like cellsIL-6proneural-mesenchymal transitionRBPJSTAT3

Identifiers

PMID32885530
PMCPMC7648018
OpenAlexW3083366886

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.