Evidence map›Paper›PMID 31889095›Full record

ArticleScientific reports2019

IL-33/ST2 axis promotes glioblastoma cell invasion by accumulating tenascin-C.

Jian-Fei Zhang, Tao Tao, Kang Wang, Guo-Xiang Zhang, Yujin Yan, Hui-Ran Lin, Yong Li, Min-Wu Guan, Jian-Jun Yu, Xin-Dong Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  13. IL-33 induces ADAMTS5 expression and cell migration in glioblastoma multiforme.Medical oncology (Northwood, London, England) · 2022
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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 5 institutions in 1 country.

Jian-Fei ZhangDepartment of Neurosurgery, the Affiliated Hospital of Medical School of Ningbo University, Ningbo, 315020, China. jefee1@yahoo.com.
Tao TaoDepartment of Health Management and Services, Ningbo Colledge of Health Science, Ningbo, 315020, China.
Kang WangDepartment of Neurosurgery, Kecheng People's Hospital, Quzhou, 324000, China.
Guo-Xiang ZhangDepartment of General Surgery, Lianshi People's Hospital, Nanxun District, Huzhou, 313013, China.
Yujin YanDepartment of Neurosurgery, the Affiliated Hospital of Medical School of Ningbo University, Ningbo, 315020, China.
Hui-Ran LinAnimal Experimental Management Center, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Yong LiDepartment of Neurosurgery, the Affiliated Hospital of Medical School of Ningbo University, Ningbo, 315020, China.
Min-Wu GuanDepartment of Neurosurgery, the Affiliated Hospital of Medical School of Ningbo University, Ningbo, 315020, China.
Jian-Jun YuDepartment of Neurosurgery, the Affiliated Hospital of Medical School of Ningbo University, Ningbo, 315020, China.
Xin-Dong WangDepartment of Neurosurgery, the Affiliated Hospital of Medical School of Ningbo University, Ningbo, 315020, China.
Ningbo University · CNChinese Academy of Sciences · CNNingbo College of Health Sciences · CNThird People's Hospital of Huzhou · CNZoucheng People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tenascin-C (TNC), a very large multimeric glycoprotein, is overexpressed in human glioblastomas, leading to a highly motile and invasive phenotype of glioma cells. However, the regulation of TNC expression in glioma has remained unclear until now. Our data suggest that interleukin-33 (IL-33) may promote the accumulation of TNC protein by autocrine or paracrine modes of action in glioma. In the present study, the expression levels of TNC, IL-33, and ST2 were measured in glioma tissue specimens, and the impact of altered IL-33 expression on TNC was investigated in vitro and in vivo. In contrast with control treatment, IL-33 treatment increased TNC expression, and knockdown of IL-33 attenuated TNC expression in glioma cells. Furthermore, IL-33 induced the activation of nuclear factor κB (NF-κB) and increased the expression of TNC in U251 cells. In addition, blockage of the IL-33-ST2-NFκB pathway resulted in downregulation of TNC production. IL-33 promoted glioma cell invasion by stimulating the secretion of TNC. Similarly, knockdown of TNC inhibited the invasiveness of glioma cells. These findings provide a novel perspective on the role of the IL-33/NF-κB/TNC signalling pathway in supporting cancer progression. Thus, targeting the IL-33/NF-κB/TNC signalling pathway may be a useful therapeutic approach in glioma.

Indexed as

Signal TransductionBiomarkersCell Line, TumorCell MovementGene ExpressionGlioblastomaHumansImmunohistochemistryInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Models, BiologicalNeoplasm InvasivenessNF-kappa BTenascinBiomarkersIL1RL1 protein, humanInterleukin-1 Receptor-Like 1 ProteinInterleukin-33NF-kappa BTenascin

Identifiers

PMID31889095
PMCPMC6937274
OpenAlexW2998532329

What OpenQuestion holds

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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.