Glioblastoma multiforme（GBM）是成人最常见的原发性恶性脑肿瘤之一。由于患者预后不良，GBM的中位生存时间通常不到1年。因此，找到在GBM治疗或预防方面具有良好预后的新治疗选择非常必要。近年来，类黄酮被频繁用于癌症治疗。它是一种新的有吸引力的分子，可以实现这种有前途的治疗选择。类黄酮已经被证明具有许多生物学功能，例如抗氧化作用、预防血管生成、抗炎作用、抑制癌细胞增殖和保护神经细胞等。它还表现出调节长链非编码RNA（LncRNA）的能力。研究证实，通过LncRNA在基因水平上，类黄酮可以调节GBM的表观遗传修饰、转录和改变miRNA（微小RNA）表达。研究还发现，通过调节LncRNA，类黄酮可以诱导GBM细胞凋亡和自噬。此外，它可以改善GBM的代谢异常，干扰肿瘤微环境和相关信号通路，并抑制GBM细胞的血管生成。最终，类黄酮可以阻止肿瘤的启动、生长、增殖、分化、侵袭和转移。在这篇综述中，我们强调了LncRNA在GBM癌症进展中的作用和类黄酮对LncRNA调节的影响，并强调它们在预防和治疗GBM中的预期作用。版权所有©2023 Elsevier Masson SAS出版。

Glioblastoma multiforme (GBM) is one of the most common primary malignant brain tumors in adults. Due to the poor prognosis of patients, the median survival time of GBM is often less than 1 year. Therefore, it is very necessary to find novel treatment options with a good prognosis for the treatment or prevention of GBM. In recent years, flavonoids are frequently used to treat cancer. It is a new attractive molecule that may achieve this promising treatment option. Flavonoids have been proved to have many biological functions, such as antioxidation, prevention of angiogenesis, anti-inflammation, inhibition of cancer cell proliferation, and protection of nerve cells. It has also shown the ability to regulate long non-coding RNA (LncRNA). Studies have confirmed that flavonoids can regulate epigenetic modification, transcription, and change microRNA (miRNA) expression of GBM through lncRNA at the gene level. It also found that flavonoids can induce apoptosis and autophagy of GBM cells by regulating lncRNA. Moreover, it can improve the metabolic abnormalities of GBM, interfere with the tumor microenvironment and related signaling pathways, and inhibit the angiogenesis of GBM cells. Eventually, flavonoids can block the tumor initiation, growth, proliferation, differentiation, invasion, and metastasis. In this review, we highlight the role of lncRNA in GBM cancer progression and the influence of flavonoids on lncRNA regulation. And emphasize their expected role in the prevention and treatment of GBM.Copyright © 2023. Published by Elsevier Masson SAS.