Tang Yi, Wang Maoru, Yu Jiangping, Lv Guangyao, Wang Yu, Yu Bin
Department of Pharmacy, Sichuan Cancer Center, Sichuan Cancer Hospital and Institute, Affiliate Cancer Hospital of University of Electronic Science and Technology of China (UESTC), Chengdu, China.
Drug Dispensing Department, Sichuan Mental Health Center, The Third Hospital of Mianyang, Mianyang, China.
Front Pharmacol. 2024 Apr 24;15:1395156. doi: 10.3389/fphar.2024.1395156. eCollection 2024.
Approximately 80% of all malignant brain tumors are gliomas, which are primary brain tumors. The most prevalent subtype of glioma, glioblastoma multiforme (GBM), is also the most deadly. Chemotherapy, immunotherapy, surgery, and conventional pharmacotherapy are currently available therapeutic options for GBM; unfortunately, these approaches only prolong the patient's life by 5 years at most. Despite numerous intensive therapeutic options, GBM is considered incurable. Accumulating preclinical data indicate that overt antitumoral effects can be induced by pharmacologically activating endocannabinoid receptors on glioma cells by modifying important intracellular signaling cascades. The complex mechanism underlying the endocannabinoid receptor-evoked antitumoral activity in experimental models of glioma may inhibit the ability of cancer cells to invade, proliferate, and exhibit stem cell-like characteristics, along with altering other aspects of the complex tumor microenvironment. The exact biological function of the endocannabinoid system in the development and spread of gliomas, however, is remains unclear and appears to rely heavily on context. Previous studies have revealed that endocannabinoid receptors are present in the tumor microenvironment, suggesting that these receptors could be novel targets for the treatment of GBM. Additionally, endocannabinoids have demonstrated anticancer effects through signaling pathways linked to the classic features of cancer. Thus, the pharmacology of endocannabinoids in the glioblastoma microenvironment is the main topic of this review, which may promote the development of future GBM therapies.
所有恶性脑肿瘤中约80%是胶质瘤,即原发性脑肿瘤。胶质瘤最常见的亚型多形性胶质母细胞瘤(GBM)也是最致命的。化疗、免疫疗法、手术和传统药物疗法是目前GBM可用的治疗选择;不幸的是,这些方法最多只能将患者的生命延长5年。尽管有众多密集的治疗选择,但GBM仍被认为无法治愈。越来越多的临床前数据表明,通过修饰重要的细胞内信号级联反应,药理学激活胶质瘤细胞上的内源性大麻素受体可诱导明显的抗肿瘤作用。在胶质瘤实验模型中,内源性大麻素受体诱发的抗肿瘤活性的复杂机制可能会抑制癌细胞的侵袭、增殖能力,并使其表现出干细胞样特征,同时改变复杂肿瘤微环境的其他方面。然而,内源性大麻素系统在胶质瘤发生和扩散中的确切生物学功能仍不清楚,而且似乎在很大程度上取决于具体情况。先前的研究表明,肿瘤微环境中存在内源性大麻素受体,这表明这些受体可能是治疗GBM的新靶点。此外,内源性大麻素已通过与癌症经典特征相关的信号通路显示出抗癌作用。因此,胶质母细胞瘤微环境中内源性大麻素的药理学是本综述的主要主题,这可能会促进未来GBM治疗方法的发展。