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Functional role of ferroptosis on cancers, activation and deactivation by various therapeutic candidates-an update.
Chemico-Biological Interactions ( IF 4.7 ) Pub Date : 2019-12-19 , DOI: 10.1016/j.cbi.2019.108930 The Hong Phong Nguyen 1 , B Mahalakshmi 2 , Bharath Kumar Velmurugan 3
Chemico-Biological Interactions ( IF 4.7 ) Pub Date : 2019-12-19 , DOI: 10.1016/j.cbi.2019.108930 The Hong Phong Nguyen 1 , B Mahalakshmi 2 , Bharath Kumar Velmurugan 3
Affiliation
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Ferroptosis is recently identified form of regulated cell death which differs from previously identified cell death in a way that it is driven by iron-dependent lipid peroxide accumulation. Morphologically, cell volume shrinkage and increased mitochondrial membrane density are main features which characterize this form of cell death. Molecular mechanism of ferroptosis induction involved suppression of the phospholipid glutathione peroxidase 4 (GPX4) and further intracellular accumulation of lipid reactive oxygen species (ROS), a process in which iron is involved; either via inhibition of system Xc- (cystine/glutamate antiporter) or direct inhibition of GPX4. Several other pathways like RAS/MAPK and NRF2 are found to be involved in ferroptosis regulation. However, the precise mechanism of ferroptosis induction is not revealed till date. Like other regulated cell deaths, ferroptosis plays important role in tumor suppression and progression as revealed by several scientific reports. This review summarizes basic information about discovery of this novel cell death mechanism including molecular mechanism of its induction and further explains the roles of ferroptosis in human cancers.
中文翻译：
铁线虫病在癌症上的功能作用，各种治疗候选物的激活和失活（更新）。
受精症是最近发现的受调节细胞死亡的形式，它不同于先前鉴定出的细胞死亡，其方式是由铁依赖性脂质过氧化物积累驱动的。从形态上讲，细胞体积缩小和线粒体膜密度增加是表征这种细胞死亡形式的主要特征。促铁作用的分子机制包括抑制磷脂谷胱甘肽过氧化物酶4（GPX4）以及脂质反应性氧（ROS）在细胞内的进一步积累，这一过程涉及铁。通过抑制系统Xc-（胱氨酸/谷氨酸逆转运蛋白）或直接抑制GPX4。发现其他几种途径（如RAS / MAPK和NRF2）也参与了促肥作用的调控。但是，直到现在还没有揭示出促肥大作用的确切机制。像其他受调节的细胞死亡一样，铁减少病在肿瘤抑制和进展中也起着重要作用，正如一些科学报告所揭示的那样。这篇综述总结了有关这种新型细胞死亡机制发现的基本信息，包括其诱导的分子机制，并进一步解释了肥大症在人类癌症中的作用。
更新日期：2019-12-19
中文翻译：
铁线虫病在癌症上的功能作用，各种治疗候选物的激活和失活（更新）。
受精症是最近发现的受调节细胞死亡的形式，它不同于先前鉴定出的细胞死亡，其方式是由铁依赖性脂质过氧化物积累驱动的。从形态上讲，细胞体积缩小和线粒体膜密度增加是表征这种细胞死亡形式的主要特征。促铁作用的分子机制包括抑制磷脂谷胱甘肽过氧化物酶4（GPX4）以及脂质反应性氧（ROS）在细胞内的进一步积累，这一过程涉及铁。通过抑制系统Xc-（胱氨酸/谷氨酸逆转运蛋白）或直接抑制GPX4。发现其他几种途径（如RAS / MAPK和NRF2）也参与了促肥作用的调控。但是，直到现在还没有揭示出促肥大作用的确切机制。像其他受调节的细胞死亡一样，铁减少病在肿瘤抑制和进展中也起着重要作用，正如一些科学报告所揭示的那样。这篇综述总结了有关这种新型细胞死亡机制发现的基本信息，包括其诱导的分子机制，并进一步解释了肥大症在人类癌症中的作用。
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