Evidence map›Paper›PMID 37408388›Full record

ArticleCNS neuroscience & therapeutics2023

Interferon-γ inducible protein 30 promotes the epithelial-mesenchymal transition-like phenotype and chemoresistance by activating EGFR/AKT/GSK3β/β-catenin pathway in glioma.

Ying Chen, Hui Xu, Pei Yu, Qing Wang, Shenggang Li, Fufu Ji, Chunwang Wu, Qing Lan

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 10 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

8 authors at 1 institution in 1 country.

Ying ChenDepartment of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China.ORCID 0000-0002-0709-3874
Hui XuDepartment of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China.
Pei YuDepartment of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China.
Qing WangDepartment of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China.
Shenggang LiDepartment of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China.
Fufu JiDepartment of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China.
Chunwang WuDepartment of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China.
Qing LanDepartment of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China.ORCID 0000-0002-8468-4942
Soochow University · CN

Funding

National Natural Science Foundation of China 81272799Suzhou City Clinical Medicine Center SZLCYXZXJ202103Suzhou Key Laboratory of Minimally Invasive Neurosurgery SZ2021262
6 · The paper itself

Abstract

aimsPrevious studies have indicated that IFI30 plays a protective role in human cancers. However, its potential roles in regulating glioma development are not fully understood.

methodsPublic datasets, immunohistochemistry, and western blotting (WB) were used to evaluate the expression of IFI30 in glioma. The potential functions and mechanisms of IFI30 were examined by public dataset analysis; quantitative real-time PCR; WB; limiting dilution analysis; xenograft tumor assays; CCK-8, colony formation, wound healing, and transwell assays; and immunofluorescence microscopy and flow cytometry.

resultsIFI30 was significantly upregulated in glioma tissues and cell lines compared with corresponding controls, and the expression level of IFI30 was positively associated with tumor grade. Functionally, both in vivo and in vitro evidence showed that IFI30 regulated the migration and invasion of glioma cells. Mechanistically, we found that IFI30 dramatically promoted the epithelial-mesenchymal transition (EMT)-like process by activating the EGFR/AKT/GSK3β/β-catenin pathway. In addition, IFI30 regulated the chemoresistance of glioma cells to temozolomide directly via the expression of the transcription factor Slug, a key regulator of the EMT-like process.

conclusionThe present study suggests that IFI30 is a regulator of the EMT-like phenotype and acts not only as a prognostic marker but also as a potential therapeutic target for temozolomide-resistant glioma.

Indexed as

beta CateninGliomaCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionErbB ReceptorsGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansInterferon-gammaPhenotypeProto-Oncogene Proteins c-aktTemozolomidebeta CateninEGFR protein, humanErbB ReceptorsGlycogen Synthase Kinase 3 betaInterferon-gammaProto-Oncogene Proteins c-aktTemozolomidechemoresistanceepithelial-mesenchymal transition-likegliomainterferon-γ inducible protein 30temozolomide

Identifiers

PMID37408388
PMCPMC10651985
OpenAlexW4383302193

What OpenQuestion holds

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LicenceCC BY
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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.