EGR3 Promotes Glioblastoma Cell Growth with Upregulation of MYC and CDK1

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 <i>MYC</i> and <i>CDK1</i> as significantly upregulated in response to EGR3 overexpression. These results suggest that EGR3 is associated with enhanced GBM cell growth, potentially through the regulation of <i>MYC</i> and <i>CDK1</i>. Our findings provide a clear model linking EGR3 to GBM proliferation and highlight MYC and CDK1 as potential therapeutic targets. This study advances the understanding of transcription factor-associated oncogenesis in GBM and suggests that targeting EGR3 may offer a novel therapeutic strategy.