Evidence map›Paper›PMID 32324311›Full record

ArticleCancer science2020

Gelsolin inhibits malignant phenotype of glioblastoma and is regulated by miR-654-5p and miR-450b-5p.

Jiakang Zhang, Takuya Furuta, Hemragul Sabit, Sho Tamai, Shabierjiang Jiapaer, Yu Dong, Masashi Kinoshita, Yasuo Uchida, Sumio Ohtsuki, Tetsuya Terasaki and 2 more

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.4field-weighted citation impact, top 21% 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, 29 citations in OpenAlex.

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  14. Liquid biomarkers in glioma.Brain tumor pathology · 2023
    Review
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  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

12 authors at 5 institutions in 2 countries.

Jiakang ZhangDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Takuya FurutaDepartment of Pathology, Kurume University, Kurume, 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.
Shabierjiang JiapaerDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Yu DongDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Masashi KinoshitaDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Yasuo UchidaGraduate School of Pharmaceutical Sciences, Tohoku University, Tohoku, Japan.
Sumio OhtsukiFaculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Tetsuya TerasakiGraduate School of Pharmaceutical Sciences, Tohoku University, Tohoku, Japan.
Shiguang ZhaoDepartment of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Mitsutoshi NakadaDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.ORCID https://orcid.org/0000-0001-9419-6101
Kanazawa University · JPTohoku University · JPHarbin Medical University · CNKumamoto University · JPKurume University · JP

Funding

Japan Agency for Medical Research and Development 20cm0106463h0002JSPS KAKENHI 16K15645JSPS KAKENHI 18H02910Kobayashi International Scholarship Foundation 66, 92The intramural clinical research grant from Kanazawa University Hospital NA
6 · The paper itself

Abstract

We have previously shown that gelsolin (GSN) levels are significantly lower in the blood of patients with glioblastoma (GBM) than in healthy controls. Here, we analyzed the function of GSN in GBM and examined its clinical significance. Furthermore, microRNAs involved in GSN expression were also identified. The expression of GSN was determined using western blot analysis and found to be significantly lower in GBM samples than normal ones. Gelsolin was mainly localized in normal astrocytes, shown using immunohistochemistry and immunofluorescence. Higher expression of GSN was correlated with more prolonged progression-free survival and overall survival. Gelsolin knockdown using siRNA and shRNA markedly accelerated cell proliferation and invasion in GBM in vitro and in vivo. The inactive form of glycogen synthase kinase-3β was dephosphorylated by GSN knockdown. In GBM tissues, the expression of GSN and microRNA (miR)-654-5p and miR-450b-5p showed an inverse correlation. The miR-654-5p and miR-450b-5p inhibitors enhanced GSN expression, resulting in reduced proliferation and invasion. In conclusion, GSN, which inhibits cell proliferation and invasion, is suppressed by miR-654-5p and miR-450b-5p in GBM, suggesting that these miRNAs can be targets for treating GBM.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationCell SurvivalDisease Models, AnimalFemaleGelsolinGene Knockout TechniquesGlioblastomaHumansMiceMicroRNAsBiomarkers, TumorGelsolinMicroRNAsMIRN450 microRNA, humanMIRN654 microRNA, humangelsolinglioblastomaGSK3βmiR-450b-5pmiR-654-5p

Identifiers

PMID32324311
PMCPMC7385387
OpenAlexW3020683859

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.