背景:IQGAP3在调节细胞增殖中起着至关重要的作用,司,和细胞骨架组织。IQGAP3的异常表达与各种肿瘤有关,但其在神经胶质瘤中的作用尚不清楚。方法:各种方法,包括遗传差异分析,单细胞分析,ROC曲线分析,Cox回归,Kaplan-Meier分析,和富集分析,被用来分析表达模式,诊断潜力,预后影响,以及正常组织和肿瘤组织中涉及IQGAP3的生物学过程。使用免疫荧光评估IQGAP3对神经胶质瘤中免疫浸润和免疫微环境的影响。此外,cBioPortal数据库用于分析IQGAP3的拷贝数变异和突变位点.还进行了实验验证以评估IQGAP3对神经胶质瘤细胞的作用并探索潜在机制。结果:IQGAP3在胶质瘤中的高表达与不良预后相关。特别是在野生型IDH和1p/19q非缺失胶质瘤中。富集分析显示IQGAP3参与调节细胞周期,PI3K/AKT信令,p53信号,和PLK1相关通路。此外,IQGAP3的表达可能与胶质母细胞瘤的免疫抑制微环境密切相关。BRD-K88742110和LY-303511是抗胶质瘤治疗中靶向IQGAP3的潜在药物。体外实验表明IQGAP3下调抑制胶质瘤细胞的增殖和迁移,PLK1/PI3K/AKT通路可能在IQGAP3介导的胶质瘤进展中发挥关键作用。结论:IQGAP3有望成为诊断的有价值的生物标志物,预后,和神经胶质瘤的免疫治疗策略。
Background:
IQGAP3 plays a crucial role in regulating cell proliferation, division, and cytoskeletal organization. Abnormal expression of
IQGAP3 has been linked to various tumors, but its function in glioma is not well understood. Methods: Various methods, including genetic differential analysis, single-cell analysis, ROC curve analysis, Cox regression, Kaplan-Meier analysis, and enrichment analysis, were employed to analyze the expression patterns, diagnostic potential, prognostic implications, and biological processes involving IQGAP3 in normal and tumor tissues. The impact of
IQGAP3 on immune infiltration and the immune microenvironment in gliomas was evaluated using immunofluorescence. Additionally, the cBioPortal database was used to analyze copy number variations and mutation sites of IQGAP3. Experimental validation was also performed to assess the effects of IQGAP3 on glioma cells and explore underlying mechanisms. Results: High
IQGAP3 expression in gliomas is associated with an unfavorable prognosis, particularly in wild-type IDH and 1p/19q non-codeleted gliomas. Enrichment analysis revealed that IQGAP3 is involved in regulating the cell cycle, PI3K/AKT signaling, p53 signaling, and PLK1-related pathways. Furthermore, IQGAP3 expression may be closely related to the immunosuppressive microenvironment of glioblastoma. BRD-K88742110 and LY-303511 are potential drugs for targeting
IQGAP3 in anti-glioma therapy. In vitro experiments showed that downregulation of IQGAP3 inhibits the proliferation and migration of glioma cells, with the PLK1/PI3K/AKT pathway potentially playing a crucial role in IQGAP3-mediated glioma progression. Conclusion: IQGAP3 shows promise as a valuable biomarker for diagnosis, prognosis, and immunotherapeutic strategies in gliomas.