替莫唑胺
GPX4
坏死性下垂
癌症研究
程序性细胞死亡
细胞凋亡
医学
胶质瘤
癌症
脂质过氧化
药理学
生物
氧化应激
内科学
谷胱甘肽过氧化物酶
过氧化氢酶
生物化学
作者
Marc Dahlmanns,Eduard Yakubov,Jana Katharina Dahlmanns
标识
DOI:10.3389/fonc.2021.783067
摘要
Glioblastoma represents the most devastating form of human brain cancer, associated with a very poor survival rate of patients. Unfortunately, treatment options are currently limited and the gold standard pharmacological treatment with the chemotherapeutic drug temozolomide only slightly increases the survival rate. Experimental studies have shown that the efficiency of temozolomide can be improved by inducing ferroptosis – a recently discovered form of cell death, which is different from apoptosis, necrosis, or necroptosis and, which is characterized by lipid peroxidation and reactive oxygen species accumulation. Ferroptosis can also be activated to improve treatment of malignant stages of neuroblastoma, meningioma, and glioma. Due to their role in cancer treatment, ferroptosis-gene signatures have recently been evaluated for their ability to predict survival of patients. Despite positive effects during chemotherapy, the drugs used to induce ferroptosis – such as erastin and sorafenib – as well as genetic manipulation of key players in ferroptosis – such as the cystine-glutamate exchanger xCT and the glutathione peroxidase GPx4 – also impact neuronal function and cognitive capabilities. In this review, we give an update on ferroptosis in different brain tumors and summarize the impact of ferroptosis on healthy tissues.
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