EGR3 Promotes Glioblastoma Cell Growth with Upregulation of MYC and CDK1.

Chia-Wei Chang, Yi-Chin Chou, Yin-Cheng Huang, Yi-Chuan Cheng

Abstract read

In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Chia-Wei ChangGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 333323, Taiwan.

Yi-Chin ChouGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 333323, Taiwan.

Yin-Cheng HuangDepartment of Neurosurgery, Chang Gung Memorial Hospital at Linkou Medical Center, Taoyuan 333423, Taiwan.

Yi-Chuan ChengGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 333323, Taiwan.ORCID 0000-0002-4772-2380

Funding

Chang Gung Medical Foundation CMRPD1M0431, CMRPD1M0432, CMRPD1P0041, CMRPD1P0042, and BMRP857 for YCC; CMRPG3N1361 for YCHNational Science and Technology Council, Taiwan MOST 110-2320-B-182 -008 -MY3 and NSTC 113-2320-B-182 -029 -MY3 for YCC; NSTC 113-2314-B-182A-132 and MOST 111-2314-B-182A-135 for YCH

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most aggressive and lethal primary brain tumor, characterized by rapid growth and resistance to therapy. Despite extensive research, the molecular mechanisms driving GBM progression remain incompletely understood. In this study, we employed integrative transcriptomic analysis to identify transcription factors associated with GBM, revealing EGR3 as a key candidate. Functional assays demonstrated that EGR3 promotes GBM cell viability, with EGR3 overexpression significantly enhancing cell growth, while EGR3 disruption impaired viability. To elucidate the downstream targets of EGR3, we further performed transcriptomic analysis and identified

Indexed as

Brain NeoplasmsCDC2 Protein KinaseEarly Growth Response Protein 3GlioblastomaProto-Oncogene Proteins c-mycCell Line, TumorCell ProliferationCell SurvivalGene Expression ProfilingGene Expression Regulation, NeoplasticHumansUp-RegulationCDC2 Protein KinaseCDK1 protein, humanEarly Growth Response Protein 3EGR3 protein, humanMYC protein, humanProto-Oncogene Proteins c-mycEGR3glioblastomatranscription factorstranscriptomic analysis

Identifiers

PMID40649712

DOI10.3390/ijms26135931

PMCPMC12249872

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LicenceCC BY

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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.