胶质瘤是最常见的原发性恶性脑肿瘤，预后差且病死率高，目前还没有有效的治疗方法。许多研究表明，复制蛋白A3（RPA3）能够调节DNA复制，RPA3的异常表达会导致基因组不稳定并诱导多种肿瘤的发展。然而，RPA3与胶质瘤之间的关系以及作用机制仍不清楚。本研究旨在探讨RPA3在胶质瘤发展中的作用及其可能的机制。我们利用中国胶质瘤基因组图谱（CGGA）、癌症基因组图谱（TCGA）和基因表达图谱库（GEO）数据库，分析RPA3的表达水平及其与临床预后的相关性。我们建立了单变量Cox回归模型来预测胶质瘤患者的预后，并分析了RPA3与免疫细胞浸润和活化之间的相关性。利用免疫组化、RT-PCR和Western blot（WB）检测了胶质瘤标本中RPA3的表达。通过转染质粒进行RPA3的敲低和过表达，研究了其对胶质瘤细胞体外增殖、迁移和侵袭能力的影响。利用WB对可能的分子机制进行了分析。结果显示，胶质瘤组织和细胞中RPA3的表达显著高于正常胶质细胞，并与胶质瘤患者的预后呈正相关。RPA3的过表达通过促进PI3K、AKT和mTOR磷酸化而激活磷脂酰肌醇3激酶（PI3K）-蛋白激酶B（AKT）-雷帕霉素靶蛋白（mTOR）信号通路，从而促进了胶质瘤细胞的增殖、迁移和侵袭。总之，RPA3在胶质瘤中高表达，并通过激活PI3K-AKT-mTOR通路促进胶质瘤的增殖、迁移和侵袭。因此，RPA3可能是胶质瘤的预后生物标志物和治疗靶点。

Gliomas are the most common primary malignant brain tumors, with a poor prognosis and high mortality, and there is no effective treatment regimen. A number of studies have shown that replication protein A3 (RPA3) can regulate DNA replication and that the abnormal expression of RPA3 can lead to genomic instability and induce the development of a variety of tumors. However, the relationship between RPA3 and gliomas and the mechanism of action remains unclear. In this study, we investigated the role of RPA3 in the development of gliomas and the possible mechanism. The Chinese Glioma Genome Atlas (CGGA), The Cancer Genome Atlas (TCGA), and the Gene Expression Omnibus (GEO) databases were used to analyze the expression level of RPA3 and its correlation with clinical prognosis. A univariate Cox regression model was established to predict the prognosis of glioma patients and analyze the correlation between RPA3 and immune cell infiltration and activation. Immunohistochemistry, RT-PCR, and Western blot (WB) were used to detect the expression of RPA3 in glioma specimens. After knocking down and overexpressing RPA3 with plasmids, effects on glioma cell proliferation, migration and invasive capacity were investigated in vitro. The possible molecular mechanisms were analyzed using WB. Results showed that the expression of RPA3 in glioma tissue and cells was significantly higher than that in normal glial cells and was positively correlated with the poor prognosis of patients with gliomas. The overexpression of RPA3 expression activated the phosphatidylinositol 3-kinase (PI3K)-AKT-mammalian target of the rapamycin (mTOR) pathway by promoting the phosphorylation of PI3K, AKT, and mTOR, thereby promoting the proliferation, migration and invasion of glioma cells. In conclusion, RPA3 is highly expressed in gliomas and promotes the proliferation, migration and invasion of gliomas by activating the PI3K-AKT-mTOR pathway. Therefore, RPA3 may be a prognostic biomarker and therapeutic target for gliomas.