Institute of Modern Physics, Chinese Academy of Sciences, 509 Nanchang Road, Lanzhou 730000, China.
Advanced Energy Science and Technology Guangdong Laboratory, Huizhou 516029, China.
Int J Mol Sci. 2021 Jan 15;22(2):817. doi: 10.3390/ijms22020817.
Cell can integrate the caspase family and mammalian target of rapamycin (mTOR) signaling in response to cellular stress triggered by environment. It is necessary here to elucidate the direct response and interaction mechanism between the two signaling pathways in regulating cell survival and determining cell fate under cellular stress. Members of the caspase family are crucial regulators of inflammation, endoplasmic reticulum stress response and apoptosis. mTOR signaling is known to mediate cell growth, nutrition and metabolism. For instance, over-nutrition can cause the hyperactivation of mTOR signaling, which is associated with diabetes. Nutrition deprivation can inhibit mTOR signaling via SH3 domain-binding protein 4. It is striking that Ras GTPase-activating protein 1 is found to mediate cell survival in a caspase-dependent manner against increasing cellular stress, which describes a new model of apoptosis. The components of mTOR signaling-raptor can be cleaved by caspases to control cell growth. In addition, mTOR is identified to coordinate the defense process of the immune system by suppressing the vitality of caspase-1 or regulating other interferon regulatory factors. The present review discusses the roles of the caspase family or mTOR pathway against cellular stress and generalizes their interplay mechanism in cell fate determination.
细胞可以整合半胱天冬酶家族和哺乳动物雷帕霉素靶蛋白(mTOR)信号通路,以响应环境触发的细胞应激。在这里,有必要阐明这两条信号通路在调节细胞存活和在细胞应激下决定细胞命运方面的直接反应和相互作用机制。半胱天冬酶家族成员是炎症、内质网应激反应和细胞凋亡的重要调节剂。mTOR 信号通路已知可介导细胞生长、营养和代谢。例如,营养过剩会导致 mTOR 信号通路的过度激活,这与糖尿病有关。营养剥夺可通过 SH3 结构域结合蛋白 4 抑制 mTOR 信号通路。引人注目的是,发现 Ras GTP 酶激活蛋白 1 以依赖半胱天冬酶的方式介导细胞存活,以抵抗不断增加的细胞应激,这描述了一种新的细胞凋亡模型。mTOR 信号通路的组成部分——雷帕霉素靶蛋白(mTOR)可以被半胱天冬酶切割,以控制细胞生长。此外,mTOR 被确定通过抑制半胱天冬酶-1 的活力或调节其他干扰素调节因子来协调免疫系统的防御过程。本综述讨论了半胱天冬酶家族或 mTOR 通路对抗细胞应激的作用,并概括了它们在细胞命运决定中的相互作用机制。