%0 Journal Article %T PI3K/Akt/mTOR信号通路与肿瘤微环境在胶质瘤研究中的进展
Advances in the PI3K/Akt/mTOR Signaling Pathway and Tumor Microenvironment in Glioma Research %A 张琪琪 %A 宋丹蕊 %A 刘嘉方 %A 喻天 %A 李缘凤 %A 何雨洪 %A 马雪超 %A 曹相玫 %J Advances in Clinical Medicine %P 1698-1705 %@ 2161-8720 %D 2025 %I Hans Publishing %R 10.12677/acm.2025.1561905 %X 胶质母细胞瘤(Glioblastoma, GBM)是一种在成人中枢神经系统(Central Nervous System, CNS)常见的,具有侵袭性的原发性脑癌。GBM的发生和发展与磷脂酰肌醇3-激酶/蛋白激酶B/雷帕霉素靶蛋白(PI3K/Akt/mTOR)信号通路的持续异常激活有密切联系。该信号通路被异常激活,能够促进肿瘤细胞增殖。这条通路也被认为影响了肿瘤微环境(Tumor Microenvironment, TME)的免疫抑制,比如PD-L1和IDO的表达增加,TGF-β和IL-10等免疫抑制因子的分泌量升高,使得肿瘤细胞更容易逃避免疫系统的清除。PI3K/Akt/mTOR通路还会影响肿瘤相关巨噬细胞(Tumor-Associated Macrophages, TAMs)的极化,刺激VEGF等血管生成因子的释放,加快TME的恶化。本文主要介绍PI3K/Akt/mTOR信号通路与TME的相互作用以及基于两者的胶质瘤治疗方法,希望为未来胶质瘤患者的治疗提供新思路。
Glioblastoma (GBM) is an aggressive primary brain cancer that is common in the central nervous system (CNS) in adults. The occurrence and progression of GBM is closely related to the persistent aberrant activation of phosphatidylinositol 3-kinase/protein kinase B/rapamycin target protein (PI3K/Akt/mTOR) signaling pathway. This signaling pathway is aberrantly activated to promote tumor cell proliferation. This pathway is also thought to affect the immunosuppression of the tumor microenvironment (TME), such as increased expression of PD-L1 and IDO, and increased secretion of immunosuppressive factors such as TGF-β and IL-10, making it easier for tumor cells to evade clearance by the immune system. The PI3K/Akt/mTOR pathway also affects the polarization of tumor-associated macrophages (TAMs), stimulates the release of angiogenic factors such as VEGF, and accelerates the deterioration of TME. This article mainly introduces the interaction between PI3K/Akt/mTOR signaling pathway and TME and the treatment of glioma based on both, hoping to provide new ideas for the treatment of glioma patients in the future. %K 胶质瘤, %K PI3K/Akt/mTOR, %K TME, %K 治疗策略, %K 免疫反应
Glioma %K PI3K/Akt/mTOR %K TME %K Therapeutic Strategies %K Immune Response %U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=118254