Abstract：
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.
摘要：
胶质母细胞瘤（GBM）仍然是最致命的原发性脑肿瘤，以惨淡的存活率为特征。迫切需要新的分子靶标来增强治疗效果。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为基因表达谱分析提供了平台,而GBM细胞系中siRNA介导的敲低和过表达测定，除了体内肿瘤发生模型，促进功能验证。发现EGFLAM在GBM组织中显著过表达,与不良预后因素和较高的肿瘤分级相关，特别是41岁以上的患者。功能测定表明EGFLAM对于维持GBM细胞增殖至关重要。生存能力，和侵入性。EGFLAM表达的敲低导致致瘤能力的显著降低。涉及EGFLAM的蛋白质组相互作用，例如NUP205，与细胞周期调节有关，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，强调其治疗潜力。该研究确定EGFLAM是GBM中的关键致癌因子，既是预后生物标志物，也是可行的治疗靶标。这些发现为未来EGFLAM靶向治疗的研究奠定了基础。旨在改善GBM患者的临床预后。
