Adaptive Changes Allow Targeting of Ferroptosis for Glioma Treatment.

GPX4 细胞凋亡 程序性细胞死亡 细胞生物学 化学 神经保护 生物 自噬 氧化应激 活性氧
作者
Renxuan Huang,Rui Dong,Nan Wang,Yichun He,Peining Zhu,Chong Wang,Beiwu Lan,Yufei Gao,Liankun Sun
出处
期刊:Cellular and Molecular Neurobiology [Springer Nature]
卷期号:: 1-20 被引量:3
标识
DOI:10.1007/s10571-021-01092-5
摘要

Ferroptosis is a type of regulated cell death that plays an essential role in various brain diseases, including cranial trauma, neuronal diseases, and brain tumors. It has been reported that cancer cells rely on their robust antioxidant capacity to escape ferroptosis. Therefore, ferroptosis exploitation could be an effective strategy to prevent tumor proliferation and invasion. Glioma is a common malignant craniocerebral tumor exhibiting complicated drug resistance and survival mechanisms, resulting in a high mortality rate and short survival time. Recent studies have determined that metabolic alterations in glioma offer exploitable therapeutic targets. These metabolic alterations allow targeted therapy to achieve some initial efficacy but have failed to inhibit glioma growth, invasion, and drug resistance effectively. It has been proposed that the reason for the high malignancy and drug resistance observed with glioma is that these tumors can effectively evade ferroptosis. Ferroptosis-inducing drugs were found to exert a positive effect by targeting this particular characteristic of glioma cells. Moreover, gliomas develop enhanced drug resistance through anti-ferroptosis mechanisms. In this study, we provided an overview of the mechanisms by which glioma aggressiveness and drug resistance are mediated by the evasion of ferroptosis. This information might provide new targets for glioma therapy as well as new insights and ideas for future research.
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