Evidence map›Paper›PMID 31617054›Full record

ArticleJournal of neuro-oncology2019

Ecotropic viral integration site 1 regulates EGFR transcription in glioblastoma cells.

Asako Mizuguchi, Shinji Yamashita, Kiyotaka Yokogami, Kazuhiro Morishita, Hideo Takeshima

Open access · hybridAbstract read
In one paragraph

Article in Journal of neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-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

4 citing papers in PubMed, 7 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

5 authors at 1 institution in 1 country.

Asako MizuguchiDepartment of Neurosurgery, Faculty of Medicine, University of Miyazaki, 5200, Kiyotake-cho, Kihara, Miyazaki-shi, Miyazaki, 889-1601, Japan. asako_mizuguchi@med.miyazaki-u.ac.jp.ORCID http://orcid.org/0000-0003-0502-4258
Shinji YamashitaDepartment of Neurosurgery, Faculty of Medicine, University of Miyazaki, 5200, Kiyotake-cho, Kihara, Miyazaki-shi, Miyazaki, 889-1601, Japan.
Kiyotaka YokogamiDepartment of Neurosurgery, Faculty of Medicine, University of Miyazaki, 5200, Kiyotake-cho, Kihara, Miyazaki-shi, Miyazaki, 889-1601, Japan.
Kazuhiro MorishitaDepartment of Tumor and Cellular Biochemistry, Faculty of Medicine, University of Miyazaki, 5200, Kiyotake-cho, Kihara, Miyazaki-shi, Miyazaki, 889-1601, Japan.
Hideo TakeshimaDepartment of Neurosurgery, Faculty of Medicine, University of Miyazaki, 5200, Kiyotake-cho, Kihara, Miyazaki-shi, Miyazaki, 889-1601, Japan.
University of Miyazaki · JP

Funding

Grant-in-Aid for Clinical Research from Miyazaki University Hospital 25462275JSPS KAKENHI 19K09486
6 · The paper itself

Abstract

purposeEcotropic viral integration site-1 (EVI1) is a transcription factor that contributes to the unfavorable prognosis of leukemia, some epithelial cancers, and glial tumors. However, the biological function of EVI1 in glioblastoma multiforme (GBM) remains unclear. Based on microarray experiments, EVI1 has been reported to regulate epidermal growth factor receptor (EGFR) transcription. Signal transduction via EGFR plays an essential role in glioblastoma. Therefore, we performed this study to clarify the importance of EVI1 in GBM by focusing on the regulatory mechanism between EVI1 and EGFR transcription.

methodsWe performed immunohistochemical staining and analyzed the EVI1-expression in glioma tissue. To determine the relationship between EVI1 and EGFR, we induced siRNA-mediated knockdown of EVI1 in GBM cell lines. To investigate the region that was essential for the EVI1 regulation of EGFR expression, we conducted promoter reporter assays. We performed WST-8 assay to investigate whether EVI1 affected on the proliferation of GBM cells or not.

resultsIt was observed that 22% of GBM tissues had over 33% of tumor cells expressing EVI1, whereas no lower-grade glioma tissue had over 33% by immunohistochemistry. In A172 and YKG1 cells, the expression levels of EGFR and EVI1 correlated. Analysis of the EGFR promoter region revealed that the EGFR promoter (from - 377 to - 266 bp) was essential for the EVI regulation of EGFR expression. We showed that EVI1 influenced the proliferation of A172 and YKG1 cells.

conclusionThis is the first study reporting the regulation of EGFR transcription by EVI1 in GBM cells.

Indexed as

AdultAgedBrain NeoplasmsErbB ReceptorsFemaleGene Expression Regulation, NeoplasticGlioblastomaHumansMaleMDS1 and EVI1 Complex Locus ProteinMiddle AgedRNA, Small InterferingEGFR protein, humanErbB ReceptorsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanRNA, Small InterferingEcotropic viral integration site-1Epidermal growth factor receptorGlioblastomaTranscription factorTyrosine kinase receptor

Identifiers

PMID31617054
PMCPMC6856030
OpenAlexW2981080598

What OpenQuestion holds

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LicenceCC BY
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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.