胶质母细胞瘤（GBM）是脑部最常见的原发性颅内肿瘤，具有高生长率和高死亡率。葫芦素 E (CUE) 是一种源自葫芦属物种的四环三萜化合物，已被证明对多种恶性肿瘤具有显着的抗肿瘤作用。在本研究中，探讨了CUE对GBM的影响及其潜在的分子机制。数据显示，CUE 以剂量和时间依赖性方式抑制 GBM 细胞系 U87-MG 和 U251-MG 的增殖。从机制上讲，CUE 在基础和表皮生长因子 (EGF) 诱导的水平上降低了粘着斑激酶 (FAK)、蛋白激酶 B (AKT) 和糖原合酶激酶 3β (GSK3β) 的磷酸化。此外，CUE 通过阻断 EGF 诱导的 FAK、AKT 和 GSK3β 磷酸化来抑制 U87-MG 和 U251-MG 细胞的增殖。随后，CUE 降低了 cyclinD1 和 cyclinB1 的表达。总的来说，这些结果表明CUE通过抑制FAK/AKT/GSK3β信号通路来抑制U87-MG和U251-MG细胞的增殖，这也表明CUE在治疗GBM中具有潜在的应用。

Glioblastoma (GBM) is the most common primary intracranial tumor in the brain with high growth rate and high mortality rate. Cucurbitacin E (CUE), a tetracyclic triterpene compound derived from species of the genus Cucurbita, has been demonstrated to display significant antitumor effects on various malignancies. In the present study, the effects of CUE on GBM and its underlying molecular mechanisms were explored. The data revealed that CUE inhibited the proliferation of the GBM cell lines U87‑MG and U251‑MG in a dose‑ and time‑dependent manner. Mechanistically, CUE reduced the phosphorylation of focal adhesion kinase (FAK), protein kinase B (AKT), and glycogen synthase kinase‑3β (GSK3β) at both basal and epidermal growth factor (EGF)‑induced levels. Moreover, CUE inhibited the proliferation of U87‑MG and U251‑MG cells by blocking EGF‑induced phosphorylation of the FAK, AKT and GSK3β. Subsequently, CUE reduced the expression of cyclinD1 and cyclinB1. Collectively, these results indicated that CUE inhibited the proliferation of U87‑MG and U251‑MG cells by suppressing the FAK/AKT/GSK3β signaling pathway, which also suggested that CUE has potential application in treating GBM.