胶质母细胞瘤（GBM）仍然是最致命的原发性脑肿瘤，其特点是生存率很低。迫切需要新的分子靶点来增强治疗效果。采用生物信息学分析和实验验证相结合的方法来研究 EGFLAM 在 GBM 中的作用。中国胶质瘤基因组图谱提供了基因表达谱分析的平台，而GBM细胞系中siRNA介导的敲低和过表达测定以及体内肿瘤发生模型促进了功能验证。研究发现 EGFLAM 在 GBM 组织中显着过度表达，与不良预后因素和较高的肿瘤分级相关，特别是在 41 岁以上的患者中。功能测定表明 EGFLAM 对于维持 GBM 细胞增殖、活力和侵袭性至关重要。 EGFLAM 表达的敲低导致致瘤能力显着下降。涉及 EGFLAM 的蛋白质组相互作用（例如与 NUP205）与细胞周期调节有关，有助于深入了解其致癌机制。体内研究进一步表明，沉默 EGFLAM 表达可以抑制肿瘤生长，强调了其治疗潜力。该研究将 EGFLAM 确定为 GBM 的关键致癌因素，既可作为预后生物标志物，又可作为可行的治疗靶点。这些发现为未来 EGFLAM 靶向疗法的研究奠定了基础，旨在改善 GBM 患者的临床结果。版权所有 © 2024。由 Elsevier B.V. 出版。

Glioblastoma (GBM) remains the most lethal primary brain tumor, characterized by dismal survival rates. Novel molecular targets are urgently required to enhance therapeutic outcomes. A combination of bioinformatics analysis and experimental validation was employed to investigate the role of EGFLAM in GBM. The Chinese Glioma Genome Atlas provided a platform for gene expression profiling, while siRNA-mediated knockdown and overexpression assays in GBM cell lines, alongside in vivo tumorigenesis models, facilitated functional validation. EGFLAM was found to be significantly overexpressed in GBM tissues, correlating with adverse prognostic factors and higher tumor grades, particularly in patients over the age of 41. Functional assays indicated that EGFLAM is vital for maintaining GBM cell proliferation, viability, and invasiveness. Knockdown of EGFLAM expression led to a marked decrease in tumorigenic capabilities. Proteomic interactions involving EGFLAM, such as with NUP205, were implicated in cell cycle regulation, providing insight into its oncogenic mechanism. In vivo studies further demonstrated that silencing EGFLAM expression could inhibit tumor growth, underscoring its therapeutic potential. The study identifies EGFLAM as a pivotal oncogenic factor in GBM, serving as both a prognostic biomarker and a viable therapeutic target. These findings lay the groundwork for future research into EGFLAM-targeted therapies, aiming to improve clinical outcomes for GBM patients.Copyright © 2024. Published by Elsevier B.V.